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  • 1.
    Axelsson, John
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Man flu is related to health communication rather than symptoms and suffering2018Ingår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 360, artikel-id k450Artikel i tidskrift (Övrigt vetenskapligt)
  • 2.
    Axelsson, John
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Sundelin, Tina
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Universitätsklinikum Essen, Germany.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    How can we improve identification of contagious individuals? Factors influencing sickness detection2018Ingår i: Proceedings of the Royal Society of London. Biological Sciences, ISSN 0962-8452, E-ISSN 1471-2954, Vol. 285, nr 1889Artikel i tidskrift (Refereegranskat)
  • 3.
    Axelsson, John
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Sundelin, Tina
    Olsson, Mats J.
    Sorjonen, Kimmo
    Axelsson, Charlotte
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Universitätsklinikum Essen, Germany.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Identification of acutely sick people and facial cues of sickness2018Ingår i: Proceedings of the Royal Society of London. Biological Sciences, ISSN 0962-8452, E-ISSN 1471-2954, Vol. 285, nr 1870, artikel-id 20172430Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Detection and avoidance of sick individuals have been proposed as essential components in a behavioural defence against disease, limiting the risk of contamination. However, almost no knowledge exists on whether humans can detect sick individuals, and if so by what cues. Here, we demonstrate that untrained people can identify sick individuals above chance level by looking at facial photos taken 2 h after injection with a bacterial stimulus inducing an immune response (2.0 ng kg-1 lipopolysaccharide) or placebo, the global sensitivity index being d' = 0.405. Signal detection analysis (receiver operating characteristic curve area) showed an area of 0.62 (95% confidence intervals 0.60-0.63). Acutely sick people were rated by naive observers as having paler lips and skin, a more swollen face, droopier corners of the mouth, more hanging eyelids, redder eyes, and less glossy and patchy skin, as well as appearing more tired. Our findings suggest that facial cues associated with the skin, mouth and eyes can aid in the detection of acutely sick and potentially contagious people.

  • 4. Brück, Emily
    et al.
    Larsson, Jacob W.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Bottai, Matteo
    Hirvikoski, Tatja
    Sundman, Eva
    Eberhardson, Michael
    Sackey, Peter
    Olofsson, Peder S.
    Lack of clinically relevant correlation between subjective and objective cognitive function in ICU survivors: a prospective 12-month follow-up study2019Ingår i: Critical Care, ISSN 1364-8535, E-ISSN 1466-609X, Vol. 23, artikel-id 253Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background

    Cognitive impairment and psychological distress are common in intensive care unit (ICU) survivors. Early identification of affected individuals is important, so intervention and treatment can be utilized at an early stage. Cognitive Failures Questionnaire (CFQ) is commonly used to screen for subjective cognitive function, but it is unclear whether CFQ scores correlate to objective cognitive function in this population.

    Methods

    Between 2014 and 2018, 100 ICU survivors aged 18–70 years from the general ICU at the Karolinska University Hospital, Solna, were included in the study. Out of these, 58 patients completed follow-up at 3 months after ICU discharge, 51 at 6 months, and 45 at 12 months. Follow-up included objective cognitive function testing using the Cambridge Neuropsychological Test Automated Battery (CANTAB) and subjective cognitive function testing with the self-rating Cognitive Failures Questionnaire (CFQ), as well as psychological self-rating with the Post-Traumatic Stress Symptoms Scale-10 (PTSS-10) and Hospital Anxiety and Depression Scale (HADS).

    Results

    The prevalence of cognitive impairment as measured by four selected CANTAB tests was 34% at 3 months after discharge, 18% at 6 months, and 16% at 12 months. There was a lack of significant correlation between CANTAB scores and CFQ scores at 3 months (r = − 0.134–0.207, p > 0.05), at 6 months (r = − 0.106–0.257, p > 0.05), and at 12 months after discharge (r = − 0.070–0.109, p > 0.05). Correlations between CFQ and PTSS-10 scores and HADS scores, respectively, were significant over the follow-up period (r = 0.372–0.710, p ≤ 0.001–0.023). In contrast, CANTAB test scores showed a weak correlation with PTSS-10 and HADS scores, respectively, at 3 months only (r = − 0.319–0.348, p = 0.008–0.015).

    Conclusion

    We found no clinically relevant correlation between subjective and objective cognitive function in this cohort of ICU survivors, while subjective cognitive function correlated significantly with psychological symptoms throughout the follow-up period. Treatment and evaluation of ICU survivors’ recovery need to consider both subjective and objective aspects of cognitive impairment, and subjective reports must be interpreted with caution as an indicator of objective cognitive function.

  • 5. Capuron, Lucile
    et al.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Institute of MedicalKarolinska Institutet, Sweden; Psychology and Behavioral Immunobiology, Germany.
    Castanon, Nathalie
    Role of Adiposity-Driven Inflammation in Depressive Morbidity2017Ingår i: Neuropsychopharmacology, ISSN 0893-133X, E-ISSN 1740-634X, Vol. 42, nr 1, s. 115-128Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Depression and metabolic disorders, including overweight and obesity, appear tightly interrelated. The prevalence of these conditions is concurrently growing worldwide, and both depression and overweight/obesity represent substantial risk factors for multiple medical complications. Moreover, there is now multiple evidence for a bidirectional relationship between depression and increased adiposity, with overweight/obesity being associated with an increased prevalence of depression, and in turn, depression augmenting the risk of weight gain and obesity. Although the reasons for this intricate link between depression and increased adiposity remain unclear, converging clinical and preclinical evidence points to a critical role for inflammatory processes and related alterations of brain functions. In support of this notion, increased adiposity leads to a chronic low-grade activation of inflammatory processes, which have been shown elsewhere to have a potent role in the pathophysiology of depression. It is therefore highly possible that adiposity-driven inflammation contributes to the development of depressive disorders and their growing prevalence worldwide. This review will present recent evidence in support of this hypothesis and will discuss the underlying mechanisms and potential therapeutic targets. Altogether, findings presented here should help to better understand the mechanisms linking adiposity to depression and facilitate the identification of new preventive and/or therapeutic strategies.

  • 6. Castanon, Nathalie
    et al.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. French National Institute for Agricultural Research (INRA), France; University of Bordeaux, France.
    Capuron, Lucile
    Neuropsychiatric comorbidity in obesity: role of inflammatory processes2014Ingår i: Frontiers in Endocrinology, ISSN 1664-2392, E-ISSN 1664-2392, Vol. 5, nr 74Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Neuropsychiatric symptoms are frequent in obesity. In addition to their substantial economic and health impact, these symptoms significantly interfere with the quality of life and social function of obese individuals. While the pathophysiological mechanisms underlying obesity-related neuropsychiatric symptoms are still under investigation and remain to be clearly identified, there is increasing evidence for a role of inflammatory processes. Obesity is characterized by a chronic low-grade inflammatory state that is likely to influence neuropsychiatric status given the well-known and highly documented effects of inflammation on brain activity/function and behavior. This hypothesis is supported by recent findings emanating from clinical investigations in obese subjects and from experimentations conducted in animal models of obesity. These studies converge to show that obesity-related inflammatory processes, originating either from the adipose tissue or gut microbiota environment, spread to the brain where they lead to substantial changes in neurocircuitry, neuroendocrine activity, neurotransmitter metabolism and activity, and neurogenesis. Together, these alterations contribute to shape the propitious bases for the development of obesity-related neuropsychiatric comorbidities.

  • 7. Castanon, Nathalie
    et al.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. French National Institute for Agricultural Research (INRA), France; University of Bordeaux, France.
    Capuron, Lucile
    Neuropsychiatric comorbidity in obesity: role of inflammatory processes2014Ingår i: Frontiers in Endocrinology, ISSN 1664-2392, E-ISSN 1664-2392, Vol. 5, artikel-id 74Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Neuropsychiatric symptoms are frequent in obesity. In addition to their substantial economic and health impact, these symptoms significantly interfere with the quality of life and social function of obese individuals. While the pathophysiological mechanisms underlying obesity-related neuropsychiatric symptoms are still under investigation and remain to be clearly identified, there is increasing evidence for a role of inflammatory processes. Obesity is characterized by a chronic low-grade inflammatory state that is likely to influence neuropsychiatric status given the well-known and highly documented effects of inflammation on brain activity/function and behavior. This hypothesis is supported by recent findings emanating from clinical investigations in obese subjects and from experimentations conducted in animal models of obesity. These studies converge to show that obesity-related inflammatory processes, originating either from the adipose tissue or gut microbiota environment, spread to the brain where they lead to substantial changes in neurocircuitry, neuroendocrine activity, neurotransmitter metabolism and activity, and neurogenesis. Together, these alterations contribute to shape the propitious bases for the development of obesity-related neuropsychiatric comorbidities.

  • 8. Göranson, Sofie Paues
    et al.
    Thålin, Charlotte
    Lundström, Annika
    Hållström, Lars
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Wallén, Håkan
    Soop, Anne
    Mobarrez, Fariborz
    Circulating H3Cit is elevated in a human model of endotoxemia and can be detected bound to microvesicles2018Ingår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, artikel-id 12641Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Early diagnosis of sepsis is crucial since prompt interventions decrease mortality. Citrullinated histone H3 (H3Cit), released from neutrophil extracellular traps (NETs) upon binding of platelets to neutrophils following endotoxin stimulation, has recently been proposed a promising blood biomarker in sepsis. Moreover, microvesicles (MVs), which are released during cell activation and apoptosis and carry a variety of proteins from their parental cells, have also been shown to be elevated in sepsis. In a randomized and placebo-controlled human model of endotoxemia (lipopolysaccharide injection; LPS), we now report significant LPS-induced elevations of circulating H3Cit in 22 healthy individuals. We detected elevations of circulating H3Cit by enzyme-linked immunosorbent assay (ELISA), as well as bound to MVs quantified by flow cytometry. H3Cit-bearing MVs expressed neutrophil and/or platelet surface markers, indicating platelet-neutrophil interactions. In addition, in vitro experiments revealed that H3Cit can bind to phosphatidylserine exposed on platelet derived MVs. Taken together; our results demonstrate that NETs can be detected in peripheral blood during endotoxemia by two distinct H3Cit-specific methods. Furthermore, we propose a previously unrecognized mechanism by which H3Cit may be disseminated throughout the vasculature by the binding to MVs.

  • 9. Henderson, Audrey J.
    et al.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Institute of Medical Psychology and Behavioral Immunobiology, Germany.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Olsson, Mats J.
    Powis, Simon J.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Perrett, David I.
    Skin colour changes during experimentally-induced sickness2017Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 60, s. 312-318Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Skin colour may be an important cue to detect sickness in humans but how skin colour changes with acute sickness is currently unknown. To determine possible colour changes, 22 healthy Caucasian participants were injected twice, once with lipopolysaccharide (LPS, at a dose of 2ng/kg body weight) and once with placebo (saline), in a randomised cross-over design study. Skin colour across 3 arm and 3 face locations was recorded spectrophotometrically over a period of 8h in terms of lightness (L(∗)), redness (a(∗)) and yellowness (b(∗)) in a manner that is consistent with human colour perception. In addition, carotenoid status was assessed as we predicted that a decrease it skin yellowness would reflect a drop in skin carotenoids. We found an early change in skin colouration 1-3h post LPS injection with facial skin becoming lighter and less red whilst arm skin become darker but also less red and less yellow. The LPS injection also caused a drop in plasma carotenoids from 3h onwards. However, the timing of the carotenoid changes was not consistent with the skin colour changes suggesting that other mechanisms, such as a reduction of blood perfusion, oxygenation or composition. This is the first experimental study characterising skin colour associated with acute illness, and shows that changes occur early in the development of the sickness response. Colour changes may serve as a cue to health, prompting actions from others in terms of care-giving or disease avoidance. Specific mechanisms underlying these colour changes require further investigation.

  • 10.
    Karshikoff, Bianka
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Sundelin, Tina
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Psykologiska institutionen, Biologisk psykologi. Karolinska Institutet, Sweden.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; University Hospital Essen, Germany.
    Role of inflammation in Human Fatigue: Relevance of Multidimensional Assessments and Potential Neuronal Mechanisms2017Ingår i: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 8, artikel-id 21Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Fatigue is a highly disabling symptom in various medical conditions. While inflammation has been suggested as a potential contributor to the development of fatigue, underlying mechanisms remain poorly understood. In this review, we propose that a better assessment of central fatigue, taking into account its multidimensional features, could help elucidate the role and mechanisms of inflammation in fatigue development. A description of the features of central fatigue is provided, and the current evidence describing the association between inflammation and fatigue in various medical conditions is reviewed. Additionally, the effect of inflammation on specific neuronal processes that may be involved in distinct fatigue dimensions is described. We suggest that the multidimensional aspects of fatigue should be assessed in future studies of inflammation-induced fatigue and that this would benefit the development of effective therapeutic interventions.

  • 11.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; University Hospital Essen, Germany.
    Alvarez-Salas, Elena
    Grigoleit, Jan-Sebastian
    Well-being and immune response: a multi-system perspective2016Ingår i: Current opinion in pharmacology (Print), ISSN 1471-4892, E-ISSN 1471-4973, Vol. 29, s. 34-41Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Whereas it is well-established that inflammation and other immune responses can change how we feel, most people are still surprised to hear that, conversely, well-being and its violations also affect our immune system. Here we show that those effects are highly adaptive and bear potential for both research and therapeutic applications. The studies discussed in this review demonstrate that immunity is tuned by ones emotions, personality, and social status as well as by other life style variables like sleep, nutrition, obesity, or exercise. We further provide a short excursion on the effects of stress and depression on immunity and discuss acute experimental endotoxemia as a model to study the effects of well-being on the innate immune response in humans.

  • 12.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Capuron, Lucile
    Chronic low-grade inflammation in metabolic disorders: relevance for behavioral symptoms.2014Ingår i: Neuroimmunomodulation, ISSN 1021-7401, E-ISSN 1423-0216, Vol. 21, nr 2-3, s. 95-101Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The ability of cytokines to influence cerebral functions and to induce the development of behavioral alterations is well established in conditions of acute or chronic high-grade activation of the innate immune system. Recent evidence suggests that the release of these immune mediators during chronic low-grade endogenous inflammatory processes may also contribute to the development of behavioral alterations. Metabolic disorders, including obesity, type 2 diabetes and the metabolic syndrome, represent examples of those conditions which are both characterized by a chronic low-grade inflammatory state and an increased prevalence of behavioral disorders. In metabolic disorders, the increased production of acute-phase proteins and cytokines (e.g. C-reactive protein, interleukin-6 and tumor necrosis factor-α), but at relatively low levels, may promote and contribute to the development of behavioral symptoms, including depressive symptoms, cognitive impairment, fatigue, sleep problems and pain. This hypothesis is supported by a growing literature referring both to experimental and clinical findings that will be reviewed here.

  • 13.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. INRA-Bordeaux University, France.
    Dexpert, S.
    Aubert, A.
    Beau, C.
    Ledaguenel, P.
    Magne, E.
    Layé, S.
    Capuron, L.
    Inflammation in the visceral adipose tissue of obese subjects: relationship with circulating inflammation and association with bariatric surgery outcomes2014Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 40, s. e29-e29Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The inflammatory state of the adipose tissue, in particular visceral adipose tissue, is believed to contribute to systemic chronic low-grade inflammation associated with obesity. Nevertheless, the precise characterization of the inflammatory profile of obese subjects, associating adipose and systemic inflammatory markers, is still needed. In addition, the question whether inflammatory specificities in obesity influence the outcomes of bariatric surgery, such as weight reduction, remains to be elucidated. To address these questions, thirty-seven obese patients were included in the present study and about 70% of them were followed up to fourteen months after bariatric surgery. Systemic concentrations of inflammatory markers were assessed using ELISA before bariatric surgery. Samples of visceral adipose tissue were extracted during bariatric surgery and gene expression of cytokines and immune cells markers were evaluated using qRT-PCR. Our results indicate that cytokines were strongly inter-correlated in the adipose tissue. In addition, we have found significant associations of adipose expression of macrophage and T cells markers with adipose expression and with systemic levels of cytokines, including TNF-α and IL-6. Importantly, a higher inflammatory state of the visceral adipose tissue before bariatric surgery predicted a lower weight reduction after surgery, notably at early stages post-surgery. Taking together, these findings highlight the importance of the inflammatory state of the visceral adipose tissue in obesity-related inflammation, and its relevance regarding its impact on outcomes of obesity treatments.

  • 14.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; University of Duisburg-Essen, Germany.
    Elsenbruch, Sigrid
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Karshikoff, Bianka
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Grigoleit, Jan-Sebastian
    Engler, Harald
    Schedlowski, Manfred
    Benson, Sven
    Mood disturbance during experimental endotoxemia: Predictors of state anxiety as a psychological component of sickness behavior2016Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 57, s. 30-37Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Lipopolysaccharide (LPS) administration is a well-established model to assess afferent immune-to-brain communication and behavioral aspects of inflammation. Nevertheless, only few studies in comparatively small samples have assessed state anxiety as a psychological component of sickness behavior despite possible clinical implications for the pathophysiology of neuropsychiatric conditions. Thus, the goal of the present analyses carried out in a large, pooled dataset from two independent study sites was to analyze the state anxiety response to LPS administration and to investigate predictors (i.e., cytokine changes; pre-existing anxiety and depression symptoms assessed with the Hospital Anxiety and Depression Scale) of the LPS-induced state anxiety changes at different time points after LPS administration. Data from 186 healthy volunteers who participated in one of six randomized, placebo-controlled human studies involving intravenous administration of LPS at doses of 0.4-0.8ng/kg body weight were combined. State anxiety as well as circulating interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-10 concentrations were significantly increased 2h and 3h after LPS administration, with a peak at 2h, and returned to baseline 6h after administration. Greater changes in IL-6 from baseline to 3h after LPS administration significantly and independently predicted a more pronounced LPS-induced state anxiety response. In addition, higher pre-existing subclinical anxiety symptoms significantly predicted a lower increase in state anxiety 3h and 6h after LPS-administration, which was mediated by TNF-α changes. In conclusion, our findings give additional support for a putative role of inflammatory mechanisms in the pathophysiology of stress-related and anxiety disorders and give new insight on the potential role of pre-existing subclinical affective symptoms.

  • 15.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Ingre, Michael
    Regenbogen, Christina
    Olsson, Mats J.
    Garke, Maria
    Brytting, Mia
    Edgar, Rachel
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Sleep during naturally occurring respiratory infections: A pilot study2019Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 79, s. 236-243Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    There is strong experimental support that infections increase the drive for sleep in animals, and it is widely believed that more sleep is part of an adaptive immune response. While respiratory infections (RI) are very prevalent in humans, there is a striking lack of systematic knowledge on how it affects sleep. We recruited 100 people, among whom 28 became sick with an RI during the study period (fulfilling criteria for influenza-like illness, ILI, or acute respiratory infection, ARI). We measured sick participants' sleep at home, both objectively (actigraphy) and subjectively (diary ratings), for one week as well as four weeks later when healthy. During the week with RI, people spent objectively longer time in bed and had a longer total sleep time compared to the healthy week. During the infection, participants also had more awakenings, but no significant differences in sleep latency or sleep efficiency. While sick, people also reported increased difficulties falling asleep, worse sleep quality, more restless sleep and more shallow sleep, while they did not report sleep to be less sufficient. Most problems occurred at the beginning of the sickness week, when symptoms were strong, and showed signs of recovery thereafter (as indicated by interactions between condition and day/night of data collection for all the 10 sleep outcomes). The degree of symptoms of RI was related to a worse sleep quality and more restless sleep, but not to any of the objective sleep outcomes or the other subjective sleep variables. Having a higher body temperature was not significantly related to any of the sleep variables. This study suggests that having a respiratory infection is associated with spending more time in bed and sleeping longer, but also with more disturbed sleep, both objectively and subjectively. This novel study should be seen as being of pilot character. There is a need for larger studies which classify pathogen type and include baseline predictors, or that manipulate sleep, in order to understand whether the sleep alterations seen during infections are adaptive and whether sleep interventions could be used to improve recovery from respiratory infections.

  • 16.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Universitätsklinikum Essen, Germany.
    Kemani, Mike K.
    Kanstrup, Marie
    Olsson, Gunnar L.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Andreasson, Anna
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Wicksell, Rikard K.
    Low-grade inflammation may moderate the effect of behavioral treatment for chronic pain in adults2016Ingår i: Journal of behavioral medicine, ISSN 0160-7715, E-ISSN 1573-3521, Vol. 39, nr 5, s. 916-924Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The purpose of the present pilot study was to explore the moderating role of basal inflammation on the effects of behavioral pain treatment in 41 patients with long-standing pain. Baseline pro-inflammatory status moderated behavioral treatment outcomes: higher pre-treatment levels of Tumor Necrosis Factor (TNF)-α and Interleukin (IL)-6 were related to less improvement in pain intensity, psychological inflexibility and in mental health-related quality of life. The treatment outcomes improved in the subgroup that had low levels of pro-inflammatory cytokines at baseline, while the subjects with higher pro-inflammatory status did not. Altogether, results indicate that low-grade inflammation may influence the behavioral treatment outcomes and provide a possible explanation of the heterogeneity in treatment response.

  • 17.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Karshikoff, Bianca
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Engler, H.
    Elsenbruch, S.
    Grigoleit, J.
    Benson, S.
    Pre-existent anxiety symptoms is associated with modified behavioral response during endotoxemia2015Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 49, s. e29-e30Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Experimental endotoxin administration is a well-established model to analyze the effect of inflammation on the development of mood impairments. However, it remains unknown from previous studies in comparatively small samples whether pre-existing inter-individual differences modulate the behavioral response during endotoxemia. We addressed this question in the present study using a merged database combining data from multiple studies performed at two study sites. In 286 healthy volunteers who either received low-dose intravenous injection of lipopolysaccharide (LPS, 0.4–0.8 ng/kg, n = 168) or saline (n = 118), plasma concentrations of TNF-alpha and IL-6 were analyzed before and 2, 3.5 and 6 hours post injection together with state anxiety symptoms (STAI). Pre-existent symptoms of anxiety and depression (HADS) were assessed before injection. LPS administration induced an increase in state anxiety 2 hours post injection that was positively correlated with increases in TNF-alpha and IL-6, but not with pre-existent HADS scores (when adjusted for age, sex, BMI, LPS dose, and study design). However, higher levels of pre-existent HADS anxiety symptoms predicted a stronger subsequent reduction in state anxiety at 3.5 and 6 hours post LPS injection. Taken together, these data suggest that although inter-individual differences in anxiety or depression symptoms do not appear to explain the extent of mood impairments during endotoxemia, at least in non-patient samples, they still lead to a modified mood response with a faster and stronger decline.

  • 18.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; University Hospital Essen, Germany.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Karshikoff, Bianka
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Stanford University School of Medicine, USA.
    Sex differences in how inflammation affects behavior: What we can learn from experimental inflammatory models in humans2018Ingår i: Frontiers in neuroendocrinology (Print), ISSN 0091-3022, E-ISSN 1095-6808, Vol. 50, s. 91-106Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Human models demonstrate that experimental activation of the innate immune system has profound effects on brain activation and behavior, inducing fatigue, worsened mood and pain sensitivity. It has been proposed that inflammation is a mechanism involved in the etiology and maintenance of depression, chronic pain and long-term fatigue. These diseases show a strong female overrepresentation, suggesting that a better understanding of sex differences in how inflammation drives behavior could help the development of individualized treatment interventions. For this purpose, we here review sex differences in studies using experimental inflammatory models to investigate changes in brain activity and behavior. We suggest a model in which inflammation accentuates sex differences in brain networks and pre-existing vulnerability factors. This effect could render women more vulnerable to the detrimental effects of immune-to-brain communication over time. We call for systematic and large scale investigations of vulnerability factors for women in the behavioral response to inflammation.

  • 19.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; University Hospital Essen, Germany.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Paues-Göranson, Sofie
    Olsson, Mats J.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Communication of health in experimentally sick men and women: A pilot study2018Ingår i: Psychoneuroendocrinology, ISSN 0306-4530, E-ISSN 1873-3360, Vol. 87, s. 188-195Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The way people communicate their ill-health and the factors involved in ill-health communication remain poorly known. In the present study, we tested how men and women communicate their sickness and assessed whether sickness-related variables (i.e., body temperature, immune response, subjective sickness symptoms) predicted communicative behaviors. Twenty-two participants were filmed during experimentally induced sickness, triggered by lipopolysaccharide administration (2ng/kg body weight), and after placebo administration, in presence of female care providers. Two trained raters scored participants' communicative behaviors (verbal complaints, moaning and sighs/deep breaths). The physiological and subjective sickness responses were similar in both sexes. Participants were more likely to moan and complain when sick, although the frequency of these behaviors remained low and no clear sex differences was observed. Nevertheless, frequency of sighs/deep breaths was increased amongst sick men but not in women. Sickness-related variables did not predict sigh/deep breath frequency. In this setting, sick men appear to display a lower threshold of expressing their malaise as compared to similarly sick women.

  • 20.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; University of Bordeaux, France; Universitätsklinikum Essen, Germany.
    Magne, Eric
    Beau, Cedric
    Aubert, Agnes
    Dexpert, Sandra
    Carrez, Julie
    Laye, Sophie
    Forestier, Damien
    Ledaguenel, Patrick
    Capuron, Lucile
    Low-grade inflammation is a major contributor of impaired attentional set shifting in obese subjects2016Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 58, s. 63-68Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Impairment in cognitive flexibility and set shifting abilities has been described in obesity. This alteration is critical as it can interfere with obesity management strategies. Recent evidences suggest that chronic low-grade inflammation may be involved in cognitive deficits associated with obesity, but the potential involvement in reduced flexibility remains unknown. The objective of this study was to assess the contribution of low-grade inflammation, determined by circulating levels of high-sensitivity C-reactive protein (hsCRP), in reduced cognitive flexibility and shifting abilities of obese subjects relatively to a group of non-obese participants. Performance in the intra/extra-dimensional set shift (IED) test, extracted from the CANTAB, was assessed in 66 obese subjects and 20 non-obese participants. Obese subjects with concentrations of hsCRP above 5 mg/L exhibited reduced performance on the IED test in comparison to obese subjects with lower levels of hsCRP and non-obese participants. This difference was particularly manifest in the number of errors made during the extra-dimensional shift (EDS errors). In contrast, performance before the extra-dimensional shift was spared. Linear regression analyses revealed that the association between obesity and IED alterations was significant only when the condition hsCRP >5 mg/L was entered in the model. These findings are important as they indicate that, rather than obesity itself, low-grade inflammation represents a major contributor of IED performance in obese subjects.

  • 21.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Magne, Eric
    Beau, Cédric
    Ledaguenel, Patrick
    Dexpert, Sandra
    Aubert, Agnès
    Layé, Sophie
    Capuron, Lucile
    Adipose inflammation in obesity: relationship with circulating levels of inflammatory markers and association with surgery-induced weight loss.2014Ingår i: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 99, nr 1, s. E53-E61Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    CONTEXT: The inflammatory state of the adipose tissue is believed to contribute to systemic low-grade inflammation in obesity.

    OBJECTIVE: This study assessed the relationship between adipose and circulating inflammatory markers as well as the influence of adipose inflammation on bariatric surgery-induced weight reduction.

    DESIGN: This was a cross-sectional and longitudinal study (up to 14 mo).

    SETTING: The study was conducted in the digestive/bariatric surgery department of the Tivoli and Jean Villar clinics, Bordeaux, France.

    PATIENTS: Thirty-seven obese patients [body mass index (BMI)>35-40 kg/m2)] seeking bariatric surgery were included. Twenty-eight of them were successively followed up at 1-3 months after surgery and 25 between 6 and 14 months after surgery.

    MAIN OUTCOME MEASURES: Fasting serum samples were collected before surgery to assess concentrations of inflammatory markers. Samples of visceral adipose tissue were extracted during surgery and gene expression of cytokines and immune cell markers were evaluated using quantitative RT-PCR. Pre- and postsurgery weight and BMI were collected.

    RESULTS: Gene expression of several cytokines were strongly intercorrelated in the visceral adipose tissue. Adipose expression of macrophage and T cell markers were related to adipose expression of TNF-α and IL-1 receptor antagonist (P<.01) and to systemic levels of TNF-α (P<.01) and IL-6 (P<.05). A higher inflammatory state of the adipose tissue predicted a lower BMI reduction after surgery (P<.05), notably at early stages after surgery.

    CONCLUSIONS: These findings support the involvement of macrophages and T cells in adipose inflammation and provide new information regarding the role of the visceral adipose tissue in the inflammatory state of obesity and its impact on obesity treatment outcomes, such as surgery-induced weight loss.

  • 22.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; University Hospital Essen, Germany.
    Petrovic, Predrag
    Olsson, Mats J.
    Paues Göranson, Sofie
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Jensen, Karin B.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Sickness behavior is not all about the immune response: Possible roles of expectations and prediction errors in the worry of being sick2018Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 74, s. 213-221Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background

    People react very differently when sick, and there are only poor correlations between the intensity of the immune response and sickness behavior. Yet, alternative predictors of the individual differences in sickness are under-investigated. Based on the predictive coding model of placebo responses, where health outcomes are function of bottom-up sensory information and top-down expectancies, we hypothesized that individual differences in behavioral changes during sickness could be explained by individual top-down expectancies and prediction errors.

    Methods

    Twenty-two healthy participants were made sick by intravenously administering lipopolysaccharide (2 ng/kg body weight). Their expectations of becoming sick were assessed before the injection.

    Results

    Participants having lower expectations of becoming sick before the injection reacted with more emotional distress (i.e., more negative affect and lower emotional arousal) than those with high expectations of becoming sick, despite having similar overall sickness behavior (i.e., a combined factor including fatigue, pain, nausea and social withdrawal). In keeping with a predictive coding model, the “prediction error signal”, i.e., the discrepancy between the immune signal and sickness expectancy, predicted emotional distress (reduction in emotional arousal in particular).

    Conclusion

    The current findings suggest that the emotional component of sickness behavior is, at least partly, shaped by top-down expectations. Helping patients having a realistic expectation of symptoms during treatment of an illness may thus reduce aggravated emotional responses, and ultimately improve patients’ quality of life and treatment compliance.

    Registration

    “Endotoxin-induced Inflammatory and Behavioral Responses and Predictors of Individual Differences”, https://clinicaltrials.gov/ct2/show/NCT02529592, registration number: NCT02529592.

  • 23.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Radun, Igor
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Magne, E
    Beau, C
    Ledaguenel, P
    Sandra, D
    Aubert, A
    Layé, S
    Capuron, L
    Visceral adipose inflammation in obesity: relationship with circulating inflammation and bariatric surgery outcomes2014Konferensbidrag (Övrigt vetenskapligt)
  • 24.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Rehman, Javaid-Ur
    Åkerstedt, Torbjörn
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Effect of long-term sleep restriction and subsequent recovery sleep on the diurnal rhythms of white blood cell subpopulations.2015Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 47, nr SI, s. 93-99Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    While acute modifications of sleep duration induces a wide array of immune function alterations, less is known of how longer periods with insufficient sleep affect immune functions and how they return to normal once recovery sleep is obtained. The purpose of the present study was to investigate the effects of five days of restricted sleep and a subsequent 7-day period of sleep recovery on white blood cell (WBC) subpopulation count and diurnal rhythms. Nine healthy males participated in a sleep protocol consisting of two baseline days (8h of sleep/night), five nights with restricted sleep (4h of sleep/night) and seven days of recovery sleep (8h of sleep/night). During nine of these days, blood was drawn hourly during night-time end every third hour during daytime, and differential WBC count was analyzed. Gradual increase across the days of sleep restriction was observed for total WBC (p<.001), monocytes (p<.001), neutrophils (p<.001) and lymphocytes (p<.05). Subsequent recovery sleep resulted in a gradual decrease in monocytes (p<.001) and lymphocytes (p=.001), but not in neutrophils that remained elevated over baseline level at the end of the 7-day recovery period. These effects were associated with altered diurnal rhythms of total WBC and neutrophils, restricted sleep being associated with higher levels during the night and at awakening, resulting in a flattening of the rhythm. The diurnal alterations were reversed when recovery sleep was allowed, although the amplitude of total WBC, neutrophils and monocytes was increased at the end of the recovery period in comparison to baseline. Altogether, these data show that long-term sleep restriction leads to a gradual increase of circulating WBC subpopulations and alterations of the respective diurnal rhythms. Although some of the effects caused by five days of restricted sleep were restored within the first days of recovery, some parameters were not back to baseline even after a period of seven recovery days.

  • 25.
    Lasselin, Julie
    et al.
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Institute of Medical Psychology and Behavioral Immunobiology, Universitätsklinikum Essen, Germany.
    Treadway, Michael T.
    Lacourt, Tamara E.
    Soop, Anne
    Olsson, Mats J.
    Karshikoff, Bianka
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Paues-Göranson, Sofie
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Dantzer, Robert
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Lipopolysaccharide Alters Motivated Behavior in a Monetary Reward Task: a Randomized Trial2017Ingår i: Neuropsychopharmacology, ISSN 0893-133X, E-ISSN 1740-634X, Vol. 42, nr 4, s. 801-810Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Inflammation-induced sickness is associated with a large set of behavioral alterations; however, its motivational aspects remain poorly explored in humans. The present study assessed the effect of lipopolysaccharide (LPS) administration at a dose of 2 ng/kg of body weight on motivation in 21 healthy human subjects in a double-blinded, placebo (saline)-controlled, cross-over design. Incentive motivation and reward sensitivity were measured using the Effort Expenditure for Rewards Task (EEfRT), in which motivation for high-effort/high-reward trials vs low-effort/low-reward trials are manipulated by variations in reward magnitude and,probability to win. Because of the strong interactions between sleepiness and motivation, the role of sleepiness was also determined. As expected, the probability to win predicted the choice to engage in high-effort/high-reward trials; however, this occurred at a greater extent after LPS than after saline administration. This effect was related to the level of sleepiness. Sleepiness increased motivation to choose the high-effort/high-reward mode of response, but only when the probability to win was the highest. LPS had no effect on reward sensitivity either directly or via sleepiness. These results indicate that systemic inflammation induced by LPS administration causes motivational changes in young healthy subjects, which are associated with sleepiness. Thus, despite its association with energy-saving behaviors, sickness allows increased incentive motivation when the effort is deemed worthwhile.

  • 26. Marraffa, Alexandre
    et al.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Solsjö, Peter
    Olsson, Mats J.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; University Hospital Essen, Germany.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Yawning, a thermoregulatory mechanism during fever? A study of yawning frequency and its predictors during experimentally induced sickness2017Ingår i: Physiology and Behavior, ISSN 0031-9384, E-ISSN 1873-507X, Vol. 182, s. 27-33Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Yawning has been proposed to serve both physiological and social functions, the latter likely to have developed later in its evolution. A central hypothesis is that yawning cools the brain but whether yawning is a thermoregulatory mechanism that is activated during hyperthermia (i.e., thermoregulatory failure) or is activated in any instance of brain temperature increase (e.g., also during fever) is unclear and experimental assessments of yawning during fever are lacking. In this study, we determined the effect of experimentally induced fever on yawning frequency. We also explored alternative predictors of yawning during sickness (sleepiness, autonomic nervous system indexes and sickness symptoms). Twenty-two healthy human subjects participated in a randomized, placebo-controlled, cross-over study, where the subjects received an injection of the bacterial endotoxin lipopolysaccharide (LPS) at a dose of 2 ng/kg body weight in one condition and placebo in the other. Yawning was scored from video recordings from 30 min before to 4 h after the injection. Body temperature was measured frequently, alongside with heart rate, blood pressure, nausea and overall sickness symptoms. Yawning frequency was found to significantly increase over time during experimentally induced sickness, but not in the placebo condition. In particular, yawning frequency was increased during the rising phase of body temperature induced by LPS administration, although no significant correlation was found between body temperature increase and yawning frequency. In addition, exploratory analyses showed that a higher yawning frequency was associated with less increase in sickness symptoms and nausea intensity. While the current study adds to previous research showing significant increase in yawning frequency during hyperthermia, further studies are needed if we are to properly characterize the brain cooling role of yawning in humans. The investigation of other functions, such as being a vasovagal inhibitory, may shed stronger light on the functions of yawning.

  • 27. Regenbogen, C.
    et al.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska institutet, Sverige; Universitätsklinikum Essen, Germany.
    Porada, D.
    Sundelin, Tina
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Psykologiska institutionen. Karolinska Institutet, Sweden.
    Peter, M.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska institutet, Sweden.
    Lundström, J. N.
    Olsson, M. J.
    Multisensory detection of sickness2016Ingår i: XXVIth Annual Meeting of the European Chemoreception Research Organization: Abstract Book, 2016, s. 94-95Konferensbidrag (Refereegranskat)
    Abstract [en]

    Converging evidence suggests that humans have a behavioral repertoire that assists the immune system in the defense against infectious disease. Behavioral detection of subtle and early sickness cues in others, and subsequent avoidance of the infected conspecific, would indeed be a cost-efficient way of coping with an environment fraught with pathogens. That humans can detect early and subtle cues of sickness by way of both olfaction and vision was recently demonstrated. The current study targeted how sickness cues affect social perception 95and how these visual and olfactory cues, alone and in unison, activate the brain.

  • 28. Regenbogen, Christina
    et al.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Universitätsklinikum Essen, Germany.
    Porada, Danja K.
    Sundelin, Tina
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Psykologiska institutionen, Biologisk psykologi. Karolinska Institutet, Sweden.
    Peter, Moa G.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institute, Sweden.
    Lundström, Johan N.
    Olsson, Mats J.
    Behavioral and neural correlates to multisensory detection of sick humans2017Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 114, nr 24, s. 6400-6405Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Throughout human evolution, infectious diseases have been a primary cause of death. Detection of subtle cues indicating sickness and avoidance of sick conspecifics would therefore be an adaptive way of coping with an environment fraught with pathogens. This study determines how humans perceive and integrate early cues of sickness in conspecifics sampled just hours after the induction of immune system activation, and the underlying neural mechanisms for this detection. In a double-blind placebo-controlled crossover design, the immune system in 22 sample donors was transiently activated with an endotoxin injection [lipopolysaccharide (LPS)]. Facial photographs and body odor samples were taken from the same donors when sick (LPS-injected) and when healthy (saline-injected) and subsequently were presented to a separate group of participants (n = 30) who rated their liking of the presented person during fMRI scanning. Faces were less socially desirable when sick, and sick body odors tended to lower liking of the faces. Sickness status presented by odor and facial photograph resulted in increased neural activation of odor-and faceperception networks, respectively. A superadditive effect of olfactory-visual integration of sickness cues was found in the intraparietal sulcus, which was functionally connected to core areas of multisensory integration in the superior temporal sulcus and orbitofrontal cortex. Taken together, the results outline a disease-avoidance model in which neural mechanisms involved in the detection of disease cues and multisensory integration are vital parts.

  • 29. Sarolidou, Georgia
    et al.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Sundelin, Tina
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; New York University, USA.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Regenbogen, Christina
    Sorjonen, Kimmo
    Lundström, Johan N.
    Stockholms universitet, Humanistiska fakulteten, Institutionen för lingvistik. Karolinska Institutet, Sweden; Monell Chemical Senses Center, USA; University of Pennsylvania, USA.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Olsson, Mats J.
    Emotional expressions of the sick face2019Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 80, s. 286-291Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    To handle the substantial threat posed by infectious diseases, behaviors that promote avoidance of contagion are crucial. Based on the fact that sickness depresses mood and that emotional expressions reveal inner states of individuals to others, which in turn affect approach/avoidance behaviors, we hypothesized that facial expressions of emotion may play a role in sickness detection. Using an experimental model of sickness, 22 volunteers were intravenously injected with either endotoxin (lipopolysaccharide; 2 ng/kg body weight) and placebo using a randomized cross-over design. The volunteers were two hours later asked to keep a relaxed expression on their face while their facial photograph was taken. To assess the emotional expression of the sick face, 49 participants were recruited and were asked to rate the emotional expression of the facial photographs of the volunteers when sick and when healthy. Our results indicate that the emotional expression of faces changed two hours after being made temporarily sick by an endotoxin injection. Sick faces were perceived as more sick/less healthy, but also as expressing more negative emotions, such as sadness and disgust, and less happiness and surprise. The emotional expressions mediated 59.1% of the treatment-dependent change in rated health. The inclusion of physical features associated with emotional expressions to the mediation analysis supported these results. We conclude that emotional expressions may contribute to detection and avoidance of infectious individuals and thereby be part of a behavioral defense against disease.

  • 30. Sarolidou, Georgia
    et al.
    Kimball, Bruce A.
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden; Universitätsklinikum Essen, Germany.
    Axelsson, John
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Lekander, Mats
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Lundström, Johan N.
    Olsson, Mats J.
    Disease detection: Volatile biomarkers in acute inflammation2017Ingår i: Chemical Senses, ISSN 0379-864X, E-ISSN 1464-3553, Vol. 42, nr 2, artikel-id P61Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Through history, infectious bacteria and viruses have posed a threat to humanity. Being able to detect and avoid pathogens is, therefore, of crucial importance. It has been shown that body odor samples, such as urine, from immune-activated animals contain sickness cues and detection of which, results in avoidance behavior in conspecifics. Perceivable changes in body odor samples have also, recently, been shown in immune-activated human participants. The main aim of this study was to identify potential volatile biomarkers of the acute inflammatory response. Healthy volunteers were injected twice in a crossover design, once with the bacterial endotoxin lipopolysaccharide (LPS, 2ng/kg bw) and once with placebo (saline). LPS caused a transient systemic inflammatory response as shown by pro-inflammatory cytocines, tympanic temperature and subjective sickness ratings (significant interactions between condition and time with all ps<.001, and all ηρ2>.663). Axillary sweat and urine were collected both before and 2–4 hours after injection. Headspace from these samples were analyzed using gas chromatography-mass spectrometry (GC-MS). GC-MS data analyses assessed the differences in the profile of volatile compounds of urine and sweat from LPS and placebo donors. Results regarding possible differences between volatile biomarkers in LPS and placebo condition will be presented and discussed.

  • 31. Thålin, Charlotte
    et al.
    Daleskog, Maud
    Paues Göransson, Sophie
    Schatzberg, Daphne
    Lasselin, Julie
    Stockholms universitet, Samhällsvetenskapliga fakulteten, Stressforskningsinstitutet. Karolinska Institutet, Sweden.
    Laska, Ann-Charlotte
    Kallner, Anders
    Helleday, Thomas
    Wallén, Håkan
    Demers, Mélanie
    Validation of an enzyme-linked immunosorbent assay for the quantification of citrullinated histone H3 as a marker for neutrophil extracellular traps in human plasma2017Ingår i: Immunologic research, ISSN 0257-277X, E-ISSN 1559-0755, Vol. 65, nr 3, s. 706-712Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    There is an emerging interest in the diverse functions of neutrophil extracellular traps (NETs) in a variety of disease settings. However, data on circulating NETs rely largely upon surrogate NET markers such as cell-free DNA, nucleosomes, and NET-associated enzymes. Citrullination of histone H3 by peptidyl arginine deiminase 4 (PAD4) is central for NET formation, and citrullinated histone H3 (H3Cit) is considered a NET-specific biomarker. We therefore aimed to optimize and validate a new enzyme-linked immunosorbent assay (ELISA) to quantify the levels of H3Cit in human plasma. A standard curve made of in vitro PAD4-citrullinated histones H3 allows for the quantification of H3Cit in plasma using an anti-histone antibody as capture antibody and an anti-histone H3 citrulline antibody for detection. The assay was evaluated for linearity, stability, specificity, and precision on plasma samples obtained from a human model of inflammation before and after lipopolysaccharide injection. The results revealed linearity and high specificity demonstrated by the inability of detecting non-citrullinated histone H3. Coefficients of variation for intra- and inter-assay variability ranged from 2.1 to 5.1% and from 5.8 to 13.5%, respectively, allowing for a high precision. Furthermore, our results support an inflammatory induction of a systemic NET burden by showing, for the first time, clear intra-individual elevations of plasma H3Cit in a human model of lipopolysaccharide-induced inflammation. Taken together, our work demonstrates the development of a new method for the quantification of H3Cit by ELISA that can reliably be used for the detection of NETs in human plasma.

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