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DePierre, Joseph W.
Alternative names
Publications (10 of 17) Show all publications
Amin, R., He, R., Gupta, D., Zheng, W., Burmakin, M., Mohammad, D. K., . . . Abedi-Valugerdi, M. (2020). The kidney injury caused by the onset of acute graft-versus-host disease is associated with down-regulation of alpha Klotho. International Immunopharmacology, 78, Article ID 106042.
Open this publication in new window or tab >>The kidney injury caused by the onset of acute graft-versus-host disease is associated with down-regulation of alpha Klotho
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2020 (English)In: International Immunopharmacology, ISSN 1567-5769, E-ISSN 1878-1705, Vol. 78, article id 106042Article in journal (Refereed) Published
Abstract [en]

Acute graft-versus-host disease (aGVHD) and kidney injury are the major complications after allogeneic hematopoietic stem cell transplantation (HSCT). Although the underlying mechanisms for the development of these complications are not yet fully understood, it has been proposed that emergence of aGVHD contributes to the development of kidney injury after HSCT. We have shown previously that aGVHD targets the kidney in a biphasic manner: at the onset, inflammatory genes are up-regulated, while when aGVHD becomes established, donor lymphocytes infiltrate the kidney. Here, we characterize renal manifestations at the onset of aGVHD. Mice receiving allogeneic bone marrow and spleen cells displayed symptoms of aGVHD and elevated serum levels of tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) within 4 days. There was concurrent kidney injury with the following characteristics: (1) elevated expression of the kidney injury biomarker, neutrophil gelatinase-associated lipocalin (NGAL), (2) accumulation of hetero-lysosomes in proximal tubule epithelial cells, and (3) reductions in alpha Klotho mRNA and protein and increased serum levels of fibroblast growth factor 23 (Fgf23), phosphate and urea. This situation resembled acute renal injury caused by bacterial lipopolysaccharide. We conclude that the onset of aGVHD is associated with kidney injury involving down-regulation of alpha Klotho, a sight that may inspire novel therapeutic approaches.

Keywords
Acute graft versus host disease, Fibroblast growth factor 23, alpha Klotho, Hematopoietic stem cell transplantation, Interferon gamma, Kidney injury, Lysosome, Tumor necrosis factor alpha
National Category
Immunology in the medical area Immunology
Identifiers
urn:nbn:se:su:diva-179641 (URN)10.1016/j.intimp.2019.106042 (DOI)000510086800002 ()31812067 (PubMedID)
Available from: 2020-03-06 Created: 2020-03-06 Last updated: 2022-02-26Bibliographically approved
Bogdanska, J., Borg, D., Bergström, U., Mellring, M., Bergman, Å., DePierre, J. & Nobel, S. (2020). Tissue distribution of C-14-labelled perfluorooctanoic acid in adult mice after 1-5 days of dietary exposure to an experimental dose or a lower dose that resulted in blood levels similar to those detected in exposed humans. Chemosphere, 239, Article ID 124755.
Open this publication in new window or tab >>Tissue distribution of C-14-labelled perfluorooctanoic acid in adult mice after 1-5 days of dietary exposure to an experimental dose or a lower dose that resulted in blood levels similar to those detected in exposed humans
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2020 (English)In: Chemosphere, ISSN 0045-6535, E-ISSN 1879-1298, Vol. 239, article id 124755Article in journal (Refereed) Published
Abstract [en]

Perfluorooctanoic acid (PFOA), a global environmental pollutant detected in both wildlife and human populations, has several pathophysiological effects in experimental animals, including hepatotoxicity, immunotoxicity, and developmental toxicity. However, details concerning the tissue distribution of PFOA, in particular at levels relevant to humans, are lacking, which limits our understanding of how humans, and other mammals, may be affected by this compound. Therefore, we characterized the tissue distribution of C-14-PFOA in mice in the same manner as we earlier examined its analogues perfluorooctanesulfonate (PFOS) and perfluorobutanesulfonate (PFBS) in order to allow direct comparisons. Following dietary exposure of adult male C57/BL6 mice for 1, 3 or 5 days to a low dose (0.06 mg/kg/day) or a higher experimental dose (22 mg/kg/day) of C-14-PFOA, both scintillation counting and whole-body autoradiography revealed the presence of PFOA in most of the 19 different tissues examined, demonstrating its ability to leave the bloodstream and enter tissues. There were no differences in the pattern of tissue distribution with the low and high dose and the tissue-to-blood ratios were similar. At both doses, PFOA levels were highest in the liver, followed by blood, lungs and kidneys. The body compartments estimated to contain the largest amounts of PFOA were the liver, blood, skin and muscle. In comparison with our identical studies on PFOS and PFBS, PFOA reached considerably higher tissue levels than PFBS, but lower than PFOS. Furthermore, the distribution of PFOA differed notably from that of PFOS, with lower tissue-to-blood ratios in the liver, lungs, kidneys and skin.

National Category
Earth and Related Environmental Sciences
Identifiers
urn:nbn:se:su:diva-176657 (URN)10.1016/j.chemosphere.2019.124755 (DOI)000498305500044 ()31726523 (PubMedID)
Available from: 2019-12-18 Created: 2019-12-18 Last updated: 2022-02-26Bibliographically approved
Calado Botelho, S., Saghafian, M., Pavlova, S., Hassan, M., DePierre, J. W. & Abedi-Valugerdi, M. (2015). Complement activation is involved in the hepatic injury caused by high-dose exposure of mice to perfluorooctanoic acid. Chemosphere, 129(SI), 225-231
Open this publication in new window or tab >>Complement activation is involved in the hepatic injury caused by high-dose exposure of mice to perfluorooctanoic acid
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2015 (English)In: Chemosphere, ISSN 0045-6535, E-ISSN 1879-1298, Vol. 129, no SI, p. 225-231Article in journal (Refereed) Published
Abstract [en]

High-dose exposure of mice to perfluorooctanoate (PFOA) induces both hepatotoxicity and immunotoxicity. Here, we characterized the effects of TO-day dietary treatment with PFOA (0.002-0.02%, w/w) on the liver and complement system of male C57BL/6 mice. At all four doses, this compound caused hepatomegaly and reduced the serum level of triglycerides (an indicator for activation of the peroxisome proliferator-activated receptor-alpha (PPAR alpha)). At the highest dose (0.02%, w/w), this hepatomegaly was associated with the hepatic injury, as reflected in increased activity of alanine aminotranferase (ALAT) in the serum, severe hepatocyte hypertrophy and hepatocellular necrosis. PFOA-induced hepatic injury was associated with in vivo activation of the complement system as indicated by (i) significant attenuation of the serum activities of both the classical and alternative pathways; (ii) a marked reduction in the serum level of the complement factor 0; and (iii) deposition of the complement factor C3 fragment (C3a) in the hepatic parenchyma. PFOA did not activate the alternative pathway of complement in vitro. At doses lower than 0.02%, PFOA induced hepatocyte hypertrophy without causing liver injury or activating complement. These results reveal substantial involvement of activation of complement in the pathogenesis of PFOA-induced hepatotoxicity.

Keywords
Complement system, Complement factor C3, Hepatotoxicity, Liver injury, Perfluorooctanoate, Peroxisome proliferator-activated receptor alpha
National Category
Biological Sciences
Identifiers
urn:nbn:se:su:diva-117762 (URN)10.1016/j.chemosphere.2014.06.093 (DOI)000353732600029 ()
Available from: 2015-06-09 Created: 2015-06-01 Last updated: 2022-02-23Bibliographically approved
Shabalina, I. G., Kramarova, T. V., Mattsson, C. L., Petrovic, N., Qazi, M. R., Csikasz, R. I., . . . Nedergaard, J. (2015). The Environmental Pollutants Perfluorooctane Sulfonate and Perfluorooctanoic Acid Upregulate Uncoupling Protein 1 (UCP1) in Brown-Fat Mitochondria Through a UCP1-Dependent Reduction in Food Intake. Toxicological Sciences, 146(2), 334-343
Open this publication in new window or tab >>The Environmental Pollutants Perfluorooctane Sulfonate and Perfluorooctanoic Acid Upregulate Uncoupling Protein 1 (UCP1) in Brown-Fat Mitochondria Through a UCP1-Dependent Reduction in Food Intake
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2015 (English)In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 146, no 2, p. 334-343Article in journal (Refereed) Published
Abstract [en]

The environmental pollutants perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) cause a dramatic reduction in the size of the major adipose tissue depots and a general body weight decrease when they are added to the food of mice. We demonstrate here that this is mainly due to a reduction in food intake; this reduction was not due to food aversion. Remarkably and unexpectedly, a large part of the effect of PFOA/PFOS on food intake was dependent on the presence of the uncoupling protein 1 (UCP1) in the mice. Correspondingly, PFOA/PFOS treatment induced recruitment of brown adipose tissue mitochondria: increased oxidative capacity and increased UCP1-mediated oxygen consumption (thermogenesis). In mice pair-fed to the food intake during PFOA/PFOS treatment in wildtype mice, brown-fat mitochondrial recruitment was also induced. We conclude that we have uncovered the existence of a regulatory component of food intake that is dependent upon brown adipose tissue thermogenic activity. The possible environmental consequences of this novel PFOA/PFOS effect (a possible decreased fitness) are noted, as well as the perspectives of this finding on the general understanding of control of food intake control and its possible extension to combatting obesity.

Keywords
thermogenesis, food restriction, adipose tissue, fatty acid oxidation, body temperature
National Category
Pharmacology and Toxicology Biological Sciences
Identifiers
urn:nbn:se:su:diva-120704 (URN)10.1093/toxsci/kfv098 (DOI)000359630300013 ()
Available from: 2015-09-18 Created: 2015-09-15 Last updated: 2022-02-23Bibliographically approved
Bogdanska, J., Sundström, M., Bergström, U., Borg, D., Abedi-Valugerdi, M., Bergman, Å., . . . Nobel, S. (2014). Tissue distribution of S-35-labelled perfluorobutanesulfonic acid in adult mice following dietary exposure for 1-5 days. Chemosphere, 98, 28-36
Open this publication in new window or tab >>Tissue distribution of S-35-labelled perfluorobutanesulfonic acid in adult mice following dietary exposure for 1-5 days
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2014 (English)In: Chemosphere, ISSN 0045-6535, E-ISSN 1879-1298, Vol. 98, p. 28-36Article in journal (Refereed) Published
Abstract [en]

Perfluorobutanesulfonyl fluoride (PBSF) has been introduced as a replacement for its eight-carbon homolog perfluorooctanesulfonyl fluoride (POSF) in the manufacturing of fluorochemicals. Fluorochemicals derived from PBSF may give rise to perfluorobutanesulfonic acid (PFBS) as a terminal degradation product. Although basic mammalian toxicokinetic data exist for PFBS, information on its tissue distribution has only been reported in one study focused on rat liver. Therefore, here we characterized the tissue distribution of PFBS in mice in the same manner as we earlier examined its eight-carbon homolog perfluorooctanesulfonate (PFOS) to allow direct comparisons. Following dietary exposure of adult male C57/BL6 mice for 1,3 or 5 d to 16 mg S-35-PFBS kg(-1) d(-1), both scintillation counting and whole-body autoradiography (WBA) revealed the presence of PFBS in all of the 20 different tissues examined, demonstrating its ability to leave the bloodstream and enter tissues. After 5 d of treatment the highest levels were detected in liver, gastrointestinal tract, blood, kidney, cartilage, whole bone, lungs and thyroid gland. WBA revealed relatively high levels of PFBS in male genital organs as well, with the exception of the testis. The tissue levels increased from 1 to 3 d of exposure but appeared thereafter to level-off in most cases. The estimated major body compartments were whole bone, liver, blood, skin and muscle. This exposure to PFBS resulted in 5-40-fold lower tissue levels than did similar exposure to PFOS, as well as in a different pattern of tissue distribution, including lower levels in liver and lungs relative to blood.

Keywords
Perfluorobutanesulfonic acid, Perfluorooctanesulfonic acid, Tissue distribution, Liquid scintillation, Autoradiography, Mice
National Category
Biological Sciences Chemical Sciences
Identifiers
urn:nbn:se:su:diva-102278 (URN)10.1016/j.chemosphere.2013.09.062 (DOI)000331679600003 ()
Note

AuthorCount:8;

Available from: 2014-04-04 Created: 2014-03-31 Last updated: 2022-02-28Bibliographically approved
Qazi, M. R., Hassan, M., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2013). Both sub-acute, moderate-dose and short-term, low-dose dietary exposure of mice to perfluorooctane sulfonate exacerbates concanavalin A-induced hepatitis. Toxicology Letters, 217(1), 67-74
Open this publication in new window or tab >>Both sub-acute, moderate-dose and short-term, low-dose dietary exposure of mice to perfluorooctane sulfonate exacerbates concanavalin A-induced hepatitis
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2013 (English)In: Toxicology Letters, ISSN 0378-4274, E-ISSN 1879-3169, Vol. 217, no 1, p. 67-74Article in journal (Refereed) Published
Abstract [en]

Exposure of rodents to perfluorooctane sulfonate (PFOS) induces pronounced hepatomegaly associated with significant alterations in hepatic histophysiology and immune status. The present investigation was designed to evaluate the effects of this perfluorochemical on immune-mediated liver damage. Accordingly, the influence of both sub-acute (10 days), moderate-dose (0.004%, w/w = 6 +/- 1.3 mg/kg body weight/day) or short-term (28 days), low-dose (0.0001%, w/w = 144 +/- 4 mu g/kg body weight/day) dietary pretreatment with PFOS on the development of concanavalin A (Con A)-induced liver damage in mice was examined. With either regimen of exposure, PFOS exacerbated the acute liver damage caused by Con A, i.e., elevated serum levels of transaminases and led to more pronounced damage of hepatic tissue. This exacerbation was associated with either reduced (moderate dose) or unaltered (low dose) hepatic levels of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma). Moreover, hepatic DNA fragmentation was enhanced, particularly following short-term exposure to a low-dose. Our findings suggest that exposure to PFOS may sensitize hepatic parenchymal cells to other insults that activate the hepatic immune system and thereby exacerbate liver damage during acute inflammation.

Keywords
Concanavalin A, Pro-inflammatory cytokines, Hepatitis, Hepatomegaly, Perfluorooctane sulfonate
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:su:diva-88276 (URN)10.1016/j.toxlet.2012.12.001 (DOI)000313708000008 ()
Note

AuthorCount:5;

Available from: 2013-03-13 Created: 2013-03-12 Last updated: 2022-02-24Bibliographically approved
Qazi, M. R., Hassan, M., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2013). Sub-acute, moderate-dose, but not short-term, low-dose dietary pre-exposure of mice to perfluorooctanoate aggravates concanavalin A-induced hepatitis. Toxicology Letters, 219(1), 1-7
Open this publication in new window or tab >>Sub-acute, moderate-dose, but not short-term, low-dose dietary pre-exposure of mice to perfluorooctanoate aggravates concanavalin A-induced hepatitis
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2013 (English)In: Toxicology Letters, ISSN 0378-4274, E-ISSN 1879-3169, Vol. 219, no 1, p. 1-7Article in journal (Refereed) Published
Abstract [en]

Exposure of mice to perfluorooctanoate (PFOA) evokes pronounced hepatomegaly along with significant alterations in both the histological structure and immune status of the liver. The present study was designed to evaluate the effects of this perfluorochemical on immune-mediated liver damage. In this connection, the influence of both sub-acute (10 days), moderate-dose (0.002% w/w = 3 +/- 0.7 mg/kg body weight/day) and short-term (28 days), low-dose (0.00005% w/w = 70 +/- 2 mu g/kg body weight/day) dietary pretreatment with PFOA on the development of concanavalin A (Con A)-induced liver damage in mice was examined. With sub-acute, moderate, but not short-term, low-dose exposure, PFOA aggravated the acute liver damage caused by Con A, i.e., elevated serum levels of transaminases and led to more pronounced damage of hepatic tissue. This aggravation was associated with significantly enhanced hepatic level of interleukin-6 (IL-6), but unaltered hepatic levels of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and interleukin-4 (IL-4). Moreover, hepatic DNA fragmentation was not changed by subacute exposure to the moderate-dose. Our findings imply that exposure to PFOA may sensitize hepatic parenchymal cells to other toxicants that activate the hepatic immune system and thereby aggravate liver injury during acute inflammation. 

Keywords
Concanavalin A, Interleukin 6, Hepatitis, Hepatomegaly, Perfluorooctanoate
National Category
Biological Sciences Pharmacology and Toxicology
Identifiers
urn:nbn:se:su:diva-89853 (URN)10.1016/j.toxlet.2013.02.017 (DOI)000317348100001 ()
Note

AuthorCount:5;

Available from: 2013-05-14 Created: 2013-05-14 Last updated: 2022-02-24Bibliographically approved
Qazi, M. R., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2012). High-dose dietary exposure of mice to perfluorooctanoate or perfluorooctane sulfonate exerts toxic effects on myeloid and B-lymphoid cells in the bone marrow and these effects are partially dependent on reduced food Consumption. Food and Chemical Toxicology, 50(9), 2955-2963
Open this publication in new window or tab >>High-dose dietary exposure of mice to perfluorooctanoate or perfluorooctane sulfonate exerts toxic effects on myeloid and B-lymphoid cells in the bone marrow and these effects are partially dependent on reduced food Consumption
2012 (English)In: Food and Chemical Toxicology, ISSN 0278-6915, E-ISSN 1873-6351, Vol. 50, no 9, p. 2955-2963Article in journal (Refereed) Published
Abstract [en]

It is well established that exposure of mice to perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) exerts adverse effects on the thymus and spleen. Here, we characterize the effects of a 10-day dietary treatment with these compounds (0.001-0.02%, w/w) on the bone marrow (BM) of mice. At a dose of 0.02%, both compounds reduced food consumption and caused atrophy of the thymus and spleen. At this same dose, histopathological and flow cytometric analysis revealed that (i) the total numbers of BM as well as the numbers of myeloid, pro/pre B, immature B and early mature B cells were all reduced significantly; and (ii) these adverse effects were reversed either partially or completely 10 days after withdrawal of these compounds. At the lower dose of 0.002%, only PFOA reduced the B-lymphoid cell population. Finally, mice fed an amount of diet equivalent to that consumed by the animals exposed to 0.02% PFOA also exhibited atrophy of the thymus and spleen, and a reduction in the number of B-lymphoid population, without affecting myeloid cells. Thus, in mice, immunotoxic doses of PFOA or PFOS induce adverse effects on the myeloid and B-lymphoid cells in the BM, in part as a consequence of reduced food consumption.

Keywords
Perfluorooctane sulfonate, Perfluorooctanoate, Bone marrow, Myeloid cells, B-lymphoid cells, Food restriction
National Category
Food Science
Identifiers
urn:nbn:se:su:diva-81257 (URN)10.1016/j.fct.2012.06.023 (DOI)000308624500001 ()
Note

AuthorCount:4;

Available from: 2012-10-15 Created: 2012-10-15 Last updated: 2022-02-24Bibliographically approved
Sundström, M., Bogdanska, J., Pham, H. V., Athanasios, V., Nobel, S., McAlees, A., . . . Bergman, Å. (2012). Radiosynthesis of perfluorooctanesulfonate (PFOS) and perfluorobutanesulfonate (PFBS), including solubility, partition and adhesion studies. Chemosphere, 87(8), 865-871
Open this publication in new window or tab >>Radiosynthesis of perfluorooctanesulfonate (PFOS) and perfluorobutanesulfonate (PFBS), including solubility, partition and adhesion studies
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2012 (English)In: Chemosphere, ISSN 0045-6535, E-ISSN 1879-1298, Vol. 87, no 8, p. 865-871Article in journal (Refereed) Published
Abstract [en]

Here, we describe for the first time the synthesis of [S-35] PFOS and [S-35] PFBS with sulfur-35 enriched sulfur dioxide as the radiolabelled reagent, resulting in 2.5 and 2.3 mCi of product, respectively. Basic information concerning the physicochemical properties of perfluorooctanesulfonate (PFOS), perfluorobutanesulfonate (PFBS) and perfluorooctanoic acid (PFOA) are still limited. Hence, we utilized these radiolabelled perfluoroalkanesulfonates (PFSAs), as well as carbon-14 labelled perfluorooctanoic acid a, ([C-14] PFOA) to determine some basic characteristics of physiological and experimental significance. The solubility of PFOS in buffered aqueous solutions at pH 7.4 was found to be severely reduced in the presence of potassium and sodium ions, which, however, did not reduce the solubility of PFOA or PFBS. PFOS was found to adhere to a small extent to polypropylene and polystyrene, whereas no such adhesion of PFOA or PFBS was detected. The extents of adhesion of PFOS and PFOA to glass were found to be 20% and 10%, respectively. For the first time, the partition coefficients for PFOS, PFBS and PFOA between n-octanol and water were determined experimentally, to be -0.7, -0.3, and 1.4, respectively, reflecting the difference in the amphiphilic natures of these molecules.

Keywords
Perfluorooctanoic acid (PFOA), Perfluoroalkyl derivatives, PFAS, Radiolabelled, Partition, Solubility
National Category
Environmental Sciences Ecology
Identifiers
urn:nbn:se:su:diva-80763 (URN)10.1016/j.chemosphere.2012.01.027 (DOI)000302988100006 ()
Note

AuthorCount:9;

Available from: 2012-09-28 Created: 2012-09-27 Last updated: 2022-02-28Bibliographically approved
Qazi, M. R., Abedi, M. R., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2011). Characterization of the Hepatic and Splenic Immune Status and Immunoglobulin Synthesis in Aged Male Mice Lacking the Peroxisome Proliferator-Activated Receptor-Alpha (PPAR alpha). Scandinavian Journal of Immunology, 73(3), 198-207
Open this publication in new window or tab >>Characterization of the Hepatic and Splenic Immune Status and Immunoglobulin Synthesis in Aged Male Mice Lacking the Peroxisome Proliferator-Activated Receptor-Alpha (PPAR alpha)
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2011 (English)In: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, Vol. 73, no 3, p. 198-207Article in journal (Refereed) Published
Abstract [en]

It is now well established that the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR alpha) is expressed in different types of immune cells and plays a pivotal role in the regulation of age-related production of inflammatory cytokines. However, the role(s) of this receptor in the regulation of immune cell homoeostasis in ageing non-lymphoid and lymphoid organs has not yet been resolved. We examine this issue here by evaluating the hepatic and splenic immune status and immunoglobulin (Ig) production in male PPAR alpha-null mice and their wild-type littermates at one and 2 years of age. In comparison with the age-matched control animals, PPAR alpha-null mice exhibited age-related elevations in the numbers of total, as well as of phenotypically distinct subpopulations of intrahepatic immune cells (IHIC) and splenocytes. Moreover, at 2 years of age, these alterations in hepatic immune cells were accompanied by significant increases in hepatic levels of the pro-inflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interferon-gamma (IFN-gamma), in combination with the development of hepatic inflammatory loci containing mixtures of leucocytes. Alterations in splenocytes of old PPAR alpha-null mice were also accompanied by increases in cellularity of both white and red pulps of the spleen. Furthermore, these same animals exhibited pronounced increases in the numbers of splenic plasma cells and enhanced production of Ig of different isotypes, including IgG1, IgG2a and IgE. Thus, our findings indicate that upon ageing, PPAR alpha plays a crucial role in regulating the total numbers, compositions and functions of immune cells in both lymphoid and non-lymphoid immune organs of mice.

National Category
Immunology
Identifiers
urn:nbn:se:su:diva-67925 (URN)10.1111/j.1365-3083.2010.02495.x (DOI)000287092100003 ()
Note
authorCount :5Available from: 2012-01-02 Created: 2012-01-02 Last updated: 2022-02-24Bibliographically approved
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