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Epithelium lining the lower female reproductive tract (FRT) acts as a barrier to pathogens and is the sentinel of the innate immune response. In particular, inflammation and breaks in epithelium integrity at the genital mucosa can promote infection with HIV and other sexually transmitted infections (STIs).
While there are several studies describing the immune modulatory effects of short chain fatty acids (SCFAs) and lactic acid in the context of the gut and cancer, respectively little is known regarding their impact on epithelium integrity and immune mediators released by vaginal, ecto- and endocervical epithelial cells of the FRT.
We have discovered lactic acid, apart from its direct antimicrobial activities, has anti-inflammatory effects on cervicovaginal epithelial cells.
To understand the global effects of lactic acid we have undertaken RNASeq analysis of cervicovaginal cells treated with lactic acid alone and in the presence of TLR ligands that mimic pathogen-associated molecular patterns to determine effects on gene expression.
This study aims to determine the mechanism of action of lactic acid informed by the RNASeq data. Findings could lead to the development of strategies to treat and prevent vaginal inflammation and consequently susceptibility to HIV, other sexually transmitted infections, and adverse reproductive health outcomes.