Abstract
Recurrent vulvovaginal infections (RVVI), a devastating group of mucosal infection, are severely affecting women's quality of life. Our understanding of the vaginal defense mechanisms have broadened recently with studies uncovering the inflammatory nature of bacterial vaginosis, inflammatory responses against novel virulence factors, innate Type 17 cells/IL-17 axis, neutrophils mediated killing of pathogens by a novel mechanism, and oxidative stress during vaginal infections. However, the pathogens have fine mechanisms to subvert or manipulate the host immune responses, hijack them and use them for their own advantage. The odds of hijacking increases, due to impaired immune responses, the net magnitude of which is the result of numerous genetic variations, present in multiple host genes, detailed in this review. Thus, by underlining the role of the host immune responses in disease etiology, modern research has clarified a major hypothesis shift in the pathophilosophy of RVVI. This knowledge can further be used to develop efficient immune-based diagnosis and treatment strategies for this enigmatic disease conditions. As for instance, plasma-derived MBL replacement, adoptive T-cell, and antibody-based therapies have been reported to be safe and efficacious in infectious diseases. Therefore, these emerging immune-therapies could possibly be the future therapeutic options for RVVI.
Highlights
Vulvovaginal infections (VVI) are the commonly reported microbiological syndrome affecting millions of women globally in all strata of society
Vaginal epithelial cells were shown to produce calcium-binding proteins namely S100A8 and S100A9 in response to C. albicans that lead to robust neutrophils migration during Vulvovaginal Candidiasis (VVC) [98, 99]
High reactive oxygen species (ROS) production plays an important role in maintaining low burden of infections, as observed in asymptomatic women depicting a strong relationship between oxidative stress and vaginal inflammation caused by Recurrent vulvovaginal infections (RVVI)
Summary
Vulvovaginal infections (VVI) are the commonly reported microbiological syndrome affecting millions of women globally in all strata of society. The resulted activation of p38/c-Fos and MKP1 signaling pathways persuades expression of pro-inflammatory cytokines and AMPs including IL-1α, IL-1β, IL-8, G-CSF, GM-CSF, β-defensin 3, CCL20, S100A8, and S100A9 from vaginal epithelial cells, which are instrumental for innate immune cells recruitment [95,96,97]. Vaginal epithelial cells were shown to produce calcium-binding proteins namely S100A8 and S100A9 in response to C. albicans that lead to robust neutrophils migration during VVC [98, 99].
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