Mechanisms of Interaction Between Yeast, Bacterial Biota, and Local Immune Response in Recurrent Vulvovaginal Candidiasis (A Review)

Vulvovaginal candidiasis (VVC) is an infection that affects up to 75% of women of reproductive age worldwide. In approximately 5–10% of women with VVC, the disease becomes chronic and relapses, with four or more exacerbations per year occurring, negatively affecting their reproductive health and quality of life. A balanced immune response and changes in vaginal biota have been shown to play a central role in maintaining mucosal homeostasis. The consequence of the disruption of this balance is the reprogramming of innate immune responses, hyperactivation of the inflammasome, as well as the difficult-to-control reproduction of Candida fungi, which, in turn, leads to the formation of recurrent VVC (RVVC). However, even though microevolutionary processes that trigger the transition of a commensal organism to a pathogen, biome translocation factors, and molecular mechanisms of interactions between its representatives and the local immune response are critical participants in the pathogenesis of the disease and are of primary importance for the development of promising therapeutic approaches to combat RVVC, they are currently insufficiently studied. The review presents information on the characteristics of the innate and adaptive immune response of the vaginal mucosa, the structure of the microbiome associated with the pathogenesis of RVVC, changes in its microecology, key molecules that determine the homeostasis of the biome and the interactions between its representatives (fungi, bacteria). The virulence factors of the fungal pathogen that determine the development of RVVC are described. The paper also discusses new potential strategies for the treatment and/or prevention of VVC based on the molecular mechanisms of interactions between yeast, vaginal bacterial biota, and the local human immune response.