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.
