Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Meningococcal DNA binds to human beta-defensin 2 and blocks its lethal effect against the bacteria
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Show others and affiliations
(English)Manuscript (preprint) (Other academic)
National Category
Microbiology
Research subject
Molecular Bioscience
Identifiers
URN: urn:nbn:se:su:diva-174760OAI: oai:DiVA.org:su-174760DiVA, id: diva2:1359563
Available from: 2019-10-09 Created: 2019-10-09 Last updated: 2019-12-04Bibliographically approved
In thesis
1. Bacteria-host cell interactions: Studies on initial colonization, antimicrobial peptides, and biofilms
Open this publication in new window or tab >>Bacteria-host cell interactions: Studies on initial colonization, antimicrobial peptides, and biofilms
2019 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The obligate human pathogen Neisseria meningitidis asymptomatically colonizes the upper respiratory tract, but crossing of the epithelial barrier can cause life-threatening meningitis and/or sepsis. N. meningitidis encounters numerous environmental challenges during colonization in the host, and has evolved different evasion strategies and virulence factors to ensure its survival. In contrast, Lactobacillus species are part of the human microbiota and their commensal colonization confers many benefits to the host, including the inhibition of pathogens.

The first cell type encountered by invading bacteria are epithelial cells and immune cells, which can effectively sense and respond to the presence of bacteria by alerting the immune system or by release of antimicrobial peptides. Antimicrobial peptides are small peptides that are able to directly kill bacteria, but also play a role in modulation of immune responses.  

This thesis focuses on the interaction between the human host and bacteria. Paper I shows that epithelial colonization by different bacterial species induces the transcription factor early growth response protein 1 (EGR1). Induction of EGR1 is mediated primarily by signaling through EGFR and ERK1/2 pathway. In paper II the ability of N. meningitidis and Lactobacillus to modulate expression of antimicrobial peptide human beta-defensin 2 (hBD2) in epithelial cells is compared. Expression of hBD2 is upregulated by lactobacilli. In contrast, N. meningitidis dampens this effect, likely mediated by induction of the host molecule A20, a negative regulator of NF-κB. Since N. meningitidis is susceptible to hBD2-mediated killing, exploitation of A20 may be an immune evasion mechanism. In paper III we demonstrate that hBD2 is able to kill N. meningitidis without causing membrane permeabilization. N. meningitidis DNA can bind hBD2 and thereby inhibit hBD2-mediated killing, presenting a possible evasion mechanism. Finally, paper IV shows that the absence of D-lactate dehydrogenase LdhA in N. meningitidis promotes aggregation and biofilm formation through increased autolysis-mediated release of extracellular DNA.

Place, publisher, year, edition, pages
Stockholm: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 2019. p. 84
Keywords
Neisseria meningitidis, Lactobacillus, host responses, EGR1, antimicrobial peptides, hBD2, A20, biofilm
National Category
Microbiology
Research subject
Molecular Bioscience
Identifiers
urn:nbn:se:su:diva-174761 (URN)978-91-7797-849-7 (ISBN)978-91-7797-850-3 (ISBN)
Public defence
2019-11-28, Vivi Täckholm-salen (Q-salen), NPQ-huset, Svante Arrhenius väg 20, Stockholm, 10:00 (English)
Opponent
Supervisors
Note

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Manuscript. Paper 3: Manuscript.

Available from: 2019-11-05 Created: 2019-10-09 Last updated: 2019-10-25Bibliographically approved

Open Access in DiVA

No full text in DiVA

Search in DiVA

By author/editor
Wassing, GabrielaSigurlásdóttir, SaraSchroeder, KristenLindås, Ann-ChristinJonas, KristinaJonsson, Ann-Beth
By organisation
Department of Molecular Biosciences, The Wenner-Gren Institute
Microbiology

Search outside of DiVA

GoogleGoogle Scholar

urn-nbn

Altmetric score

urn-nbn
Total: 15 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf