An altered immunity hypothesis for the development of symptomatic bacterial vaginosis

Clin Infect Dis. 2007 Feb 15;44(4):554-7. doi: 10.1086/511045. Epub 2007 Jan 5.


The hypothesis is advanced that the transition from a Lactobacillus-dominated vaginal microflora to a microflora characteristic of bacterial vaginosis (BV), as well as development of the adverse consequences of BV in some women but not in others, are due to alterations in innate immunity. A microbial-induced inhibition of Toll-like receptor expression and/or activity may block induction of proinflammatory immunity and lead to the proliferation of atypical vaginal bacteria. A lack of 70-kDa heat-shock protein production and release in response to abnormal flora would compound this failure to activate antimicrobial immune responses. A deficit in vaginal mannose-binding lectin concentrations would further decrease the capacity for microbial killing and increase the likelihood of bacterial migration from the vagina to the upper genital tract.

Publication types

  • Review

MeSH terms

  • Adult
  • Female
  • Gardnerella vaginalis / isolation & purification
  • Humans
  • Immunity, Innate / physiology
  • Immunocompetence
  • Immunocompromised Host*
  • Lactobacillus / immunology
  • Lactobacillus / physiology*
  • Middle Aged
  • Prognosis
  • Risk Assessment
  • Severity of Illness Index
  • Toll-Like Receptor 4 / immunology*
  • Toll-Like Receptor 4 / metabolism
  • Vaginosis, Bacterial / immunology*
  • Vaginosis, Bacterial / physiopathology


  • TLR4 protein, human
  • Toll-Like Receptor 4