One can propose a possible immunologic link between BV and VVC with the high community diversity and dysbiosis characteristic of BV, inducing genital mucosal proinflammatory cytokine concentrations (IL-1, IL-8, IL-16, TNF-α, INF gamma, MCP-1) transforming commensal Candida organisms but also reacting to the new fungal threat so inducing an inflammatory vulvovaginitis clinical response [2,20,21,45,46]. This evidence concerns the gene CXCL8 and bacterial vaginosis.