Inflammatory response during human vaginal infection with Candida albicans

Introduction. The microbiological, pathological and clinical factors determining vaginal candidiasis and recurrent vaginal candidiasis have long been studied, particularly using rodent models. The validity of which for understanding the pathogenesis of disease in women has been questioned. The most prevalent agent is critically determined by activation of microbial and host factors leading to persistent vaginal inflammation coupled to the inability of the inflammatory cells to resolve the fungal infection. Here we studied the activation of inflammasome complex neutrophil-recruiting and activating cytokines in the vaginal secretion of women with clinically established vaginal candidiasis. Materials and methods. In human vaginal samples positive for C. albicans with vaginal candidiasis (n=20) and carriage (n=15), infiltration of neutrophils, inflammatory mediators such as IL-8 and IL-1β, activation of inflammasome complex and expression of aspartyl proteases (SAPs) were examined. Results. In vaginal swabs of patients with vaginal candidiasis we found: i) consistent recruitment of neutrophils; ii) appreciable level of IL-8 and IL-1β; iii) activation of inflammasome complex; iv) consistent expression of SAP2, SAP5 and SAP6. Conclusions. These results show that immunopathogenesis of vaginal candidiasis is mediated by local recruitment of neutrophils, inflammatory cytokines secretion and inflammasome activation that mirror the upregulation of SAP2, SAP5 and SAP6 gene expression.