Candida Vaginitis: When Opportunism Knocks, the Host Responds

Brian M Peters,Mairi C Noverr,Junko Yano,Paul L Fidel,Kasturi Haldar

doi:10.1371/journal.ppat.1003965

Brian M Peters, Mairi C Noverr + Show 3 more

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https://doi.org/10.1371/journal.ppat.1003965

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Abstract

Candida Vaginitis: When Opportunism Knocks, the Host Responds

Highlights

Candida albicans, an opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide [1]
While exhaustive efforts have found no major role for adaptive immunity in susceptibility to vaginitis, recent studies have identified the importance of innate immunity in regulating vaginitis symptomatology
A family of calcium-binding proteins termed S100A8 and S100A9 ‘‘alarmins’’ have been implicated in the innate vaginal epithelial cell response to C. albicans [18]. Because these proteins have vigorous polymorphonuclear leukocyte (PMN) chemotactic activity, it was hypothesized that epithelial expression of S100s may play a key role in controlling PMN migration into the vaginal lumen. While this was confirmed, studies using mice lacking expression of S100A8/9 proteins determined that these factors were sufficient but not necessary for driving the PMN response [19]

Summary

Introduction

An opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide [1]. While exhaustive efforts have found no major role for adaptive immunity in susceptibility to vaginitis, recent studies have identified the importance of innate immunity in regulating vaginitis symptomatology. While this was confirmed, studies using mice lacking expression of S100A8/9 proteins determined that these factors were sufficient but not necessary for driving the PMN response [19].

Results

Conclusion