Contribution of TLR2 pathways in the pathogenesis of Vulvovaginal candidiasis.

RODRIGUEZ EMILSE; GARCÍA LN; RIERA F; VIGEZZI C; PAINETTI N; CAEIRO JP; MIRÓ MS; ICELY PA; MALDONADO C; SOTOMAYOR CE

Pathogen and Disease

Oxford University Press

Lugar: Londres; Año: 2017 vol. 75 p. 45 - 55

Candida albicans is the prevalent etiological agent in acute vulvovaginal infection and the most severe chronic conditionknown as recurrent vulvovaginal candidiasis (VVC). A critical role of local innate immunity in defense and pathogenesis ofvaginal infection by Candida is proposed. The fungal recognition by the innate immune receptor is an essential step for theinduction of local responses including cytokines and antimicrobial peptides (AMPs) production for host protection. UsingTLR2-deficient mice, we characterized the early innate immune response during VVC. Intravaginal challenge of TLR2−/−mice with C. albicans demonstrated that in response to the initial massive penetration, a strong local inflammatory reactionwith recruitment of polymorphonuclear neutrophils was developed. Both interleukin 1β (IL1β)?regarded as the hallmark ofVVC immunopathogenesis?and IL6 were increased in vaginal lavage. Murine beta defensin 1 (mBD1), a constitutive AMPwith fungicidal and chemotactic activity, was significantly upregulated in wild type (WT) animals in response to infection.Interestingly, in the absence of TLR2 recognition, levels of mBD1 RNA more than twice higher than those in WT infectedanimals were observed. Interestingly, our results demonstrate that TLR2 signaling is important to control the fungal burdenin the vaginal tract. These finding provide new evidence about the role of this innate receptor during VVC.