Contribution of TLR2 pathway in the pathogenesis of vulvovaginal candidiasis

MIRÓ, MARÍA SOLEDAD; RODRÍGUEZ, EMILSE; VIGEZZI, CECILIA; ICELY, PAULA ALEJANDRA; GARCÍA, LUCIANA N.; PAINETTI, NAHUEL; MALDONADO, CRISTINA A.; RIERA, FERNANDO OSCAR; CAEIRO, JUAN PABLO; SOTOMAYOR, CLAUDIA ELENA

Pathogens and Disease

Oxford University Press

Año: 2017 vol. 75

andida albicans is the prevalent etiological agent in acute vulvovaginal infection and the most severe chronic condition known as recurrent vulvovaginal candidiasis (VVC). A critical role of local innate immunity in defense and pathogenesis of vaginal infection by Candida is proposed. The fungal recognition by the innate immune receptor is an essential step for the induction of local responses including cytokines and antimicrobial peptides (AMPs) production for host protection. Using TLR2-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 reaction with recruitment of polymorphonuclear neutrophils was developed. Both interleukin 1β (IL1β)-regarded as the hallmark of VVC immunopathogenesis-and IL6 were increased in vaginal lavage. Murine beta defensin 1 (mBD1), a constitutive AMP with fungicidal and che