Journal Article

An Altered Immunity Hypothesis for the Development of Symptomatic Bacterial Vaginosis

Steven S. Witkin, Iara M. Linhares, Paulo Giraldo and William J. Ledger

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 44, issue 4, pages 554-557
Published in print February 2007 | ISSN: 1058-4838
Published online February 2007 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/511045
An Altered Immunity Hypothesis for the Development of Symptomatic Bacterial Vaginosis

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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.

Journal Article.  2761 words. 

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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