ROLE OF S100 CALCIUM-BINDING PROTEINS AS NEUTROPHIL CHEMOTACTIC FACTORS INVOLVED IN THE IMMUNOPATHOGENESIS OF VULVOVAGINAL CANDIDIASIS
Document Type
Presentation
Start Date
22-10-2010 10:30 AM
End Date
22-10-2010 10:45 AM
Description
Background: Vulvovaginal candidiasis (WC) caused by Candida species is a common mucosa! infection affecting significant numbers of women during their reproductive years. While adaptive immunity and innate resistance by polymorphonuclear neutrophils (PMNs) have no protective role against WC, a robust PMN migration into the vagina occurs in susceptible women, resulting in an acute inflammatory reaction. The PMN migration is strongly correlated to the vaginal presence of S100A8 and S100A9 calcium-binding proteins (CBPs) during symptomatic infection. The purpose of this study was to characterize the role of S100 CBPs in the immunopathogenesis of VVC using the established mouse model.
Methods: Vaginal lavage fluid from inoculated mice with Candida was tested for PMN chemotactic activity and the presence of S100A8 and S100A9 CBPs by Western blot and ELISA. Expression of S100 CBPs and a series of pattern recognition receptors (PRRs) in vaginal epithelial cells was evaluated by immunostaining and qPCR.
Results: Compared to inoculated mice with low vaginal PMNs, those with high PMNs showed that: (i) vaginal lavage fluid exhibited higher PMN chemotactic activity and had elevated levels of S100A8 and S100A9 CBPs, (ii) the production of S100 CBPs by vaginal epithelial cells was upregulated, (iii) expression of mannose receptor and SIGNR1, but not TLR2, TLR4 or dectin-1, was increased. Finally, PMN chemotactic activity of lavage fluid was abrogated following neutralization with anti-S100A8, but not anti-S100A9, antibodies.
Conclusion: These data suggest that vaginal epithelial cells in susceptible hosts exhibit PRR activation by Candida and produce S100 CBPs responsible for the acute inflammatory response associated with WC.
Recommended Citation
Yano, Junko and Fidel, P. L. Jr., "ROLE OF S100 CALCIUM-BINDING PROTEINS AS NEUTROPHIL CHEMOTACTIC FACTORS INVOLVED IN THE IMMUNOPATHOGENESIS OF VULVOVAGINAL CANDIDIASIS" (2010). Dr. Joseph M. Moerschbaecher, III Graduate Research Day. 9.
https://digitalscholar.lsuhsc.edu/grad_rs/2010/presentation1/9
ROLE OF S100 CALCIUM-BINDING PROTEINS AS NEUTROPHIL CHEMOTACTIC FACTORS INVOLVED IN THE IMMUNOPATHOGENESIS OF VULVOVAGINAL CANDIDIASIS
Background: Vulvovaginal candidiasis (WC) caused by Candida species is a common mucosa! infection affecting significant numbers of women during their reproductive years. While adaptive immunity and innate resistance by polymorphonuclear neutrophils (PMNs) have no protective role against WC, a robust PMN migration into the vagina occurs in susceptible women, resulting in an acute inflammatory reaction. The PMN migration is strongly correlated to the vaginal presence of S100A8 and S100A9 calcium-binding proteins (CBPs) during symptomatic infection. The purpose of this study was to characterize the role of S100 CBPs in the immunopathogenesis of VVC using the established mouse model.
Methods: Vaginal lavage fluid from inoculated mice with Candida was tested for PMN chemotactic activity and the presence of S100A8 and S100A9 CBPs by Western blot and ELISA. Expression of S100 CBPs and a series of pattern recognition receptors (PRRs) in vaginal epithelial cells was evaluated by immunostaining and qPCR.
Results: Compared to inoculated mice with low vaginal PMNs, those with high PMNs showed that: (i) vaginal lavage fluid exhibited higher PMN chemotactic activity and had elevated levels of S100A8 and S100A9 CBPs, (ii) the production of S100 CBPs by vaginal epithelial cells was upregulated, (iii) expression of mannose receptor and SIGNR1, but not TLR2, TLR4 or dectin-1, was increased. Finally, PMN chemotactic activity of lavage fluid was abrogated following neutralization with anti-S100A8, but not anti-S100A9, antibodies.
Conclusion: These data suggest that vaginal epithelial cells in susceptible hosts exhibit PRR activation by Candida and produce S100 CBPs responsible for the acute inflammatory response associated with WC.