Atopobium vaginae triggers an innate immune response in an in vitro model of bacterial vaginosis
Bacterial vaginosis is the most common vaginal disorder among women of reproductive age. The pathogenesis of bacterial vaginosis is poorly understood, but is defined by a transition in the vaginal flora from the predominant Lactobacillus species to other bacterial species such as Atopobium vaginae a...
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Published in | Microbes and infection Vol. 10; no. 4; pp. 439 - 446 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Lausanne
Elsevier SAS
01.04.2008
Amsterdam Elsevier Paris |
Subjects | |
Online Access | Get full text |
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Summary: | Bacterial vaginosis is the most common vaginal disorder among women of reproductive age. The pathogenesis of bacterial vaginosis is poorly understood, but is defined by a transition in the vaginal flora from the predominant
Lactobacillus species to other bacterial species such as
Atopobium vaginae and
Gardnerella vaginalis. This change is associated with an increase in vaginal cytokine secretion. We hypothesize that vaginal epithelial cells respond to bacterial vaginosis-associated bacteria by triggering an innate immune response. We observed that vaginal epithelial cells secreted interleukin-6 and interleukin-8 in response to
Atopobium vaginae and
Gardnerella vaginalis, but not to
Lactobacillus crispatus.
Atopobium vaginae induced increased levels of interleukin-6 and interleukin-8 transcripts, as well as increased transcripts for the antimicrobial peptide β-defensin 4. This innate immune response required live bacteria capable of protein synthesis in direct contact with vaginal epithelial cells. The response of vaginal epithelial cells was mediated by Toll-like receptor 2, required the adaptor protein MyD88, and involved activation of the NFκB signaling pathway. These results suggest that
Atopobium vaginae stimulates an innate immune response from vaginal epithelial cells, leading to localized cytokine and defensin production, and possibly contributes to the pathogenesis of bacterial vaginosis. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1286-4579 1769-714X |
DOI: | 10.1016/j.micinf.2008.01.004 |