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Title: Bacteroides fragilis inhibits Candida albicans induced IL-17
Authors: Stappers, M. H. T.
Janssen, N. A. F.
Joosten, L. A. B.
Netea, M. G.
Issue Date: 2011
Source: CYTOKINE, 56(1). p. 93-93
Abstract: Background: Bacteroids fragilis and Candida albicans are both part of the commensal intestinal flora. When B. fragilis spreads to normally sterile parts of the body it is a potent inducer of abscess formation. These abscesses are often polymicrobial and synergistic effects in promoting larger abscesses and bacterial persistence have been observed for bacterial co-infections. In contrast, the presence of fungi in abscesses and the effect of fungal and microbial co-infections on the host immune response has been poorly studied. The aim of this study was to assess the modulatory effect of B. Fragilis on the C. albicans induced cytokine profile. Methods: Peripheral blood mononuclear cells (PBMCs) from healthy volunteers were stimulated with heat- killed B. fragilis (107/ml), heat- killed C. albicans (105/ ml), or the combination and cytokine levels were determined in supernatants by ELISA. Results: Both B. fragilis (107/ml) and C. albicans (105/ml) are potent inducers of IL-8 and IL-6, with a moderate IL-1b and TNFa production, while induction of IL-23, IFNc and IL-10 is low. In contrast to B. fragilis, C. albicans is a potent inducer of IL-17. Coincubation of Bacteroides fragilis and C. albicans resulted in a significant decrease of IL- 17 secretion by PBMCs, whereas co-incubation had an additive effect on most other cytokines. B. fragilis inhibited IL-17 production even if added to the cells two hours after stimulation with C. albicans. B. fragilis induced these effects through Toll-like receptor 2 (TLR2), and the TLR2 stimulus Pam3Cys had similar inhibitory effects on C. albicans-induced IL-17 secretion. Conclusion: B. fragilis inhibits C. albicans induced IL-17 secretion through TLR2-mediated signalling. This finding may have important consequences for the patho-physiology of bacterial-fungal mixed abscesses, as well as during co-colonization of the intestinal mucosa with these two microorganisms.
Notes: Radboud Univ Nijmegen, Dept Med, Med Ctr, NL-6525 ED Nijmegen, Netherlands. Radboud Univ Nijmegen, Nijmegen Inst Infect Inflammat & Immun N4i, Med Ctr, NL-6525 ED Nijmegen, Netherlands. Canisius Wilhelmina Hosp, Dept Med Microbiol & Infect Dis, Nijmegen, Netherlands. Hasselt Univ, Diepenbeek, Belgium.
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ISSN: 1043-4666
e-ISSN: 1096-0023
DOI: 10.1016/j.cyto.2011.07.272
ISI #: 000295437800317
Category: M
Type: Journal Contribution
Appears in Collections:Research publications

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