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DOI 10.1097/qco.0000000000000620

Медицинская библиотека · Current opinion in infectious diseases · 2020

Host-vaginal microbiota interactions in the pathogenesis of bacterial vaginosis.

Muzny Christina A, Łaniewski Paweł, Schwebke Jane R, Herbst-Kralovetz Melissa M

СтатьяПоддержка NIH: внешняя программаОбзорПеревод пока не подготовлен

Аннотация

PURPOSE OF REVIEW: The cause of bacterial vaginosis, the most common cause of vaginal discharge in women, remains controversial. We recently published an updated conceptual model on bacterial vaginosis pathogenesis, focusing on the roles of Gardnerella vaginalis and Prevotella bivia as early colonizers and Atopobium vaginae and other bacterial vaginosis-associated bacteria (BVAB) as secondary colonizers in this infection. In this article, we extend the description of our model to include a discussion on the role of host-vaginal microbiota interactions in bacterial vaginosis pathogenesis.

RECENT FINDINGS: Although G. vaginalis and P. bivia are highly abundant in women with bacterial vaginosis, neither induce a robust inflammatory response from vaginal epithelial cells. These early colonizers may be evading the immune system while establishing the bacterial vaginosis biofilm. Secondary colonizers, including A. vaginae, Sneathia spp., and potentially other BVAB are more potent stimulators of the host-immune response to bacterial vaginosis and likely contribute to its signs and symptoms as well as its adverse outcomes.

SUMMARY: Elucidating the cause of bacterial vaginosis has important implications for diagnosis and treatment. Our current bacterial vaginosis pathogenesis model provides a framework for key elements that should be considered when designing and testing novel bacterial vaginosis diagnostics and therapeutics.

Для цитирования: Muzny Christina A, Łaniewski Paweł, Schwebke Jane R, Herbst-Kralovetz Melissa M. Host-vaginal microbiota interactions in the pathogenesis of bacterial vaginosis.. Current opinion in infectious diseases. 2020. DOI: 10.1097/qco.0000000000000620.

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