TABLE 1.

Microbial and immunological changes associated with bacterial vaginosis

Microbiological or immunological change(s) (reference[s])
Increased microbial diversity
Transition to a Nugent score of 7–10; increased abundance of small Gram-variable rods or Gram-negative rods and curved Gram-variable rods (40, 211)
Diverse with low Lactobacillus abundance, typically characterized by decreased prevalence of CST I (L. crispatus dominant), CST II (L. gasseri), CST III (L. iners), and CST V (L. jensenii) and increased prevalence of CST IV (higher relative abundances of BVAB1, G. vaginalis, A. vaginae, and Prevotella spp., etc.) (2, 4, 212)
Soluble biomarkers
Increased vaginal pH (4, 213)
Lower l- and d-lactic acid concn (74)
Lower AMP (including α-defensins, HBD-2, and SLPI) concn (59)
Higher 12-hydroxyeicosatetraenoic acid (58) and SCFA (60, 61) levels
Polymicrobial biofilm formation by inflammatory bacteria such as G. vaginalis, A. vaginae, P. bivia, and/or F. nucleatum (113, 114, 119)
Changes in genital inflammation profile
Overall increase in cytokines and chemokines, with the exception of IP-10, MIG, GRO, CCL22, MIP-1α, and GM-CSF (2, 4, 42, 44)
Increased levels of MMPs (45–47)
Immune cells and humoral immunity
Phenotypic changes in APCs (2)
Maturation and activation of monocyte-derived DCs (CD40, CD83, and HLADR) (49)
Increased no. and activation of mucosal CD4+ T cells (CD69 and CCR5) (26, 57)
IgA response to G. vaginalis cytolysin (53)
Metaproteomic changes
Decrease in epithelial barrier integrity, cytoskeletal alterations, and cell membrane biological processes; reduced cell wall organization and peptidoglycan biosynthesis (26, 112, 214)
Host genetics
Polymorphisms in inflammatory cytokines (e.g., IL-1β, IL-10, IL-5, IL-6, and TNF-α) and Toll-like receptor (e.g., TLR-2, -4, and -7) genes (107–110)