Abstract
The immunological response to bacterial vaginosis (BV) remains poorly understood and recurrent BV is still a major public health burden especially in the pregnant population. This article reviews the potential mechanisms by which BV-associated bacteria suppress and circumvent the host and microbial defence responses, and propagate their survival/dominance without overt inflammation. We discuss the composition of cervicovaginal mucosal barrier and the mechanism by which BV circumvents host defence: the degradation of the mucosal barrier and immunoglobulin A (IgA); the BV-associated organism Gardnerella vaginalis haemolysin (vaginolysin); diminished IgA response against vaginolysin; mucosal sialic acid degradation, foraging and depletion; inhibition of IL-8-induced neutrophilic infiltration; and metabolite-induced incapacitation of neutrophil and monocyte chemotaxis. We also highlight the tolerance/resistance to both host and antimicrobial molecules mounted by BV-associated biofilms. A plausible role of sialic acid-binding immunoglobulin-like lectins (SIGLECS) was also suggested. Sialidase, which is often produced by G. vaginalis , is central to the immunosuppression, relapse and recurrence observed in BV, although it is supported by other hydrolytic enzymes, vaginolysin and immunomodulatory metabolites.