An altered immunity hypothesis for the development of symptomatic bacterial vaginosis.
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.
Witkin
Steven S
SS
Department of Obstetrics and Gynecology, Weill Medical College of Cornell University, New York, NY 10021, USA. switkin@med.cornell.edu
Linhares
Iara M
IM
Giraldo
Paulo
P
Ledger
William J
WJ
D000328:Adult; D005260:Female; D006194:Gardnerella vaginalis / Q000302:isolation & purification; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D007121:Immunocompetence; D016867:Immunocompromised Host; D007778:Lactobacillus / Q000276:immunology / Q000502:physiology*; D008875:Middle Aged; D011379:Prognosis; D018570:Risk Assessment; D012720:Severity of Illness Index; D051197:Toll-Like Receptor 4 / Q000276:immunology* / Q000378:metabolism; D016585:Vaginosis, Bacterial / Q000276:immunology* / Q000503:physiopathology
C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4