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2018 ; 86
(2
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Candidalysin Drives Epithelial Signaling, Neutrophil Recruitment, and
Immunopathology at the Vaginal Mucosa
#MMPMID29109176
Richardson JP
; Willems HME
; Moyes DL
; Shoaie S
; Barker KS
; Tan SL
; Palmer GE
; Hube B
; Naglik JR
; Peters BM
Infect Immun
2018[Feb]; 86
(2
): ä PMID29109176
show ga
Unlike other forms of candidiasis, vulvovaginal candidiasis, caused primarily by
the fungal pathogen Candida albicans, is a disease of immunocompetent and
otherwise healthy women. Despite its prevalence, the fungal factors responsible
for initiating symptomatic infection remain poorly understood. One of the
hallmarks of vaginal candidiasis is the robust recruitment of neutrophils to the
site of infection, which seemingly do not clear the fungus, but rather exacerbate
disease symptomatology. Candidalysin, a newly discovered peptide toxin secreted
by C. albicans hyphae during invasion, drives epithelial damage, immune
activation, and phagocyte attraction. Therefore, we hypothesized that
Candidalysin is crucial for vulvovaginal candidiasis immunopathology.
Anti-Candida immune responses are anatomical-site specific, as effective
gastrointestinal, oral, and vaginal immunities are uniquely compartmentalized.
Thus, we aimed to identify the immunopathologic role of Candidalysin and
downstream signaling events at the vaginal mucosa. Microarray analysis of C.
albicans-infected human vaginal epithelium in vitro revealed signaling pathways
involved in epithelial damage responses, barrier repair, and leukocyte
activation. Moreover, treatment of A431 vaginal epithelial cells with
Candidalysin induced dose-dependent proinflammatory cytokine responses (including
interleukin 1? [IL-1?], IL-1?, and IL-8), damage, and activation of c-Fos and
mitogen-activated protein kinase (MAPK) signaling, consistent with fungal
challenge. Mice intravaginally challenged with C. albicans strains deficient in
Candidalysin exhibited no differences in colonization compared to isogenic
controls. However, significant decreases in neutrophil recruitment, damage, and
proinflammatory cytokine expression were observed with these strains. Our
findings demonstrate that Candidalysin is a key hypha-associated virulence
determinant responsible for the immunopathogenesis of C. albicans vaginitis.
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