Glycan Profile Alterations in Vaginitis and Their Role in Pathogen-Host Interactions

Glycosylation is one of the post-translational modifications that occur in the endoplasmic reticulum (ER)-Golgi pathway. During enzymatic glycosylation, glycosidic linkages form between saccharides, proteins and lipids. Cervicovaginal mucus (CVM), produced by epithelial cells in the female genital tract, is predominantly composed of water, mucins, and immunologically active factors. CVM is a viscoelastic natural hydrogel that lubricates the vagina and acts as a barrier against microorganisms. The glycan compounds of CVM function as cellular recognition, adherence and signaling molecules, as well as mediating host-microbe interactions. Additionally, the endocervical and vaginal epithelia secrete cervicovaginal fluid (CVF), which contains glycan compounds and various antimicrobial agents. The vaginal epithelium is mainly colonized by lactic acid bacteria (LAB) in a state of eubiosis. These bacteria produce immunomodulatory and antimicrobial compounds to prevent vaginitis. Disturbing vaginal eubiosis can lead to changes in the microbial community and the development of inflammation. Pathogens possess various mechanisms and virulence factors that facilitate their virulence. A significant proportion of microbial mechanisms and pathogen-host interactions are linked to glycan structural functions. Changes in the glycan profile are associated with vaginitis and may result from bacterial glycosidase activity, which compromises vaginal mucus and epithelial integrity. The aim of this review is to describe the glycan composition of CVF in eubiosis and dysbiosis, the influence of pathogens on glycan profiles, immune system regulation, and glycan-dependent factors in pathogen-host interactions. Understanding glycan-dependent events during vaginitis could be crucial for identifying new glycan biomarkers and treatment targets for vaginitis.