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Review
. 2014 Apr 3;10(4):e1003965.
doi: 10.1371/journal.ppat.1003965. eCollection 2014 Apr.

Candida vaginitis: when opportunism knocks, the host responds

Brian M Peters  1 , Junko Yano  2 , Mairi C Noverr  3 , Paul L Fidel Jr  2
Affiliations
Review

Candida vaginitis: when opportunism knocks, the host responds

Brian M Peters et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Working model of the immunopathogenesis of C. albicans vaginitis.
(A) Yeast forms of C. albicans asymptomatically colonize the vaginal epithelium despite the presence of numerous pattern recognition receptors (PRR) on the epithelial surface. (B) C. albicans begins to undergo the yeast-to-hypha switch under morphogenesis-inducing conditions (increases in estrogen, elevated vaginal pH, and microbiota disruption). Augmented recognition by PRRs, increased hyphal biomass, and expression of hypha-associated virulence factors elicits inflammatory signaling (S100A8/9 alarmins and proinflammatory cytokines) in the vaginal epithelium, resulting in initial migration of PMNs from the lamina propria (L.P.) to the vaginal lumen. (C) Failure to adequately reduce immunopathological triggers results in the continued expression of innate immune effectors by the vaginal epithelium. These initial signals, coupled with secondary amplification of immune effectors by recruited PMNs, contribute to symptomatic infection and characteristic immunopathology.
See this image and copyright information in PMC

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