Vaginal immunity in response to microbial perturbation is still poorly understood and may be crucial for protection from adverse outcomes associated with bacterial vaginosis (BV). BV is the most prevalent vaginal disorder in adult women worldwide. However, its pathogenesis is still elusive. In BV-positive women, inflammatory signs are scant--approximately 50% of women are asymptomatic. The number of vaginal neutrophils in the BV-positive patient is not increased with respect to healthy women. In contrast, vaginal interleukin (IL)-1beta levels are largely increased. Recent findings indicate that microbial hydrolytic enzymes could be responsible for dampening the expected proinflammatory response cascade after IL-1beta increase. In other words, BV causes a large increase of vaginal IL-1beta, which is not paralleled by an increase of IL-8 levels, suggesting that BV-associated factors specifically dampen IL-8. The impairment of IL-8 increase may explain the absence of neutrophil increase in most women exposed to a massive abnormal anaerobic vaginal colonization (BV). Among BV-positive women, vaginal innate immunity is strongly correlated to a specific adaptive immune response: the immunoglobulin A (IgA) against the hemolysin produced by Gardnerella vaginalis (anti-Gvh IgA), which is the main bacterium present in BV. High anti-Gvh IgA levels are protective for adverse pregnancy outcomes. However, an exaggerated inflammatory response, mainly attributed to genetic polymorphisms, is also implicated in BV-associated adverse outcomes.
