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ABSTRACT
Secretory aspartyl proteinases (Saps) of Candida albicans are key virulence traits which cause inflammasome-dependent, aseptic inflammation in a mouse model of vaginitis. In this paper, neutrophil migration in response to Sap2, Sap6 and chemo-attractive products released from Sap-treated vaginal epithelium was measured in vitro, ex vivo and in vivo. Our results show that Sap2 and Sap6 induce neutrophil migration and production of potent chemoattractive chemokines such as IL-8 and MIP-2 by vaginal epithelial cells. Our data suggest that at least part of MIP-2 production depends upon IL-1β activity. The vaginal fluid of Candida-infected mice contained a heat-labile inhibitor of neutrophil candidacidal activity that was absent from the vaginal fluid of Sap-treated mice. Overall, our data provide additional information on the capacity of C. albicans Saps to cause aseptic vaginal inflammation and highlight the potential role of some chemokines released from vaginal epithelial cells in this phenomenon.
Abbreviations
| ATP | = | adenosine triphosphate |
| H. I. | = | heat inactivated |
| Sap | = | Secretory aspartyl proteinase |
Disclosure of potential conflicts of interest
No potential conflicts of interest were disclosed.
Acknowledgments
We kindly thank Mario Amacker, Christian Moser and Matthias Kaeser for providing recombinant, enzymatically-active Sap2 and tSap2.
Funding
This work was supported by “FondazioneCassa di Risparmio 2012.0128.021.” The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.