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Cited by 59

The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.

Role of TLR1, TLR2 and TLR6 in the modulation of intestinal inflammation and Candida albicans elimination

Choteau, Laura, Vancraeyneste, Hélène, Le Roy, Didier, Dubuquoy, Laurent, Romani, Luiginia, Jouault, Thierry, Poulain, Daniel, Sendid, Boualem, Calandra, Thierry, Roger, Thierry, Jawhara, Samir·2017·Gut Pathogens
DOI 10.1186/s13099-017-0158-0
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Abstract

Toll-like receptors (TLRs) are the major pattern recognition receptors that mediate sensing of a wide range of microorganisms. TLR2 forms heterodimers with either TLR1 or TLR6, broadening its ligand diversity against pathogens. TLR1, TLR2 and TLR6 have been implicated in the recognition of Candida albicans , an opportunistic fungal pathogen that colonizes the gastrointestinal tract. In this study, we explored whether the deficiency in TLR1, TLR2 or TLR6 impacts C. albicans colonization and inflammation-associated colonic injury in the dextran sulfate sodium (DSS)-induced colitis in mice. DSS treatment and C. albicans challenge induced greater weight loss, worse clinical signs of inflammation, higher histopathologic scores, and increased mortality rates in TLR1 −/− and TLR2 −/− mice when compared to TLR6 −/− and wild-type mice. The number of C. albicans colonies in the stomach, colon and feces was decreased in TLR6 −/− mice as compared to TLR2 −/− , TLR1 −/− and wild-type mice. Interestingly, the population of E. coli in colonic luminal contents, intestinal permeability to FITC-dextran and cytokine expression were significantly increased in TLR1 −/− and TLR2 −/− mice, while they were decreased in TLR6 −/− mice. In contrast to TLR6, both TLR1 and TLR2 deficiencies increased intestinal inflammation, and the overgrowth of C. albicans and E. coli populations in the colitis model, suggesting the involvement of TLR1 and TLR2 in epithelial homeostasis, and a role of TLR6 in increasing intestinal inflammation in response to pathogen-sensing.

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Metadata

Authors
Choteau, L., Vancraeyneste, H., Le Roy, D., Dubuquoy, L., Romani, L., Jouault, T., Poulain, D., Sendid, B., Calandra, T., Roger, T., & Jawhara, S.
Venue
Gut Pathogens
Publisher
Springer Science and Business Media LLC
Published
2017-02-15
Volume
9
Issue
1
ISSN
1757-4749
DOI
10.1186/s13099-017-0158-0
Cited by
59
References
57
Language
en
Funders
  • ‘‘ALLFUN’’ project ‘‘Fungi in the setting of inflammation, allergy and auto-immune diseases: translating basic science into clinical practices (FP7 Health 260338)
  • Swiss National Science Foundation (320030_149511 and 310030_138488)
  • the Faculty of Biology and Medicine from the University of Lausanne (Interdisciplinary grant CellAirTox to TR)

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