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Review
. 2016 Aug 15;214 Suppl 1(Suppl 1):S29-35.
doi: 10.1093/infdis/jiw140. Epub 2016 Apr 7.

The Interplay of Host Immunity, Environment and the Risk of Bacterial Vaginosis and Associated Reproductive Health Outcomes

Kerry Murphy  1 , Caroline M Mitchell  2
Affiliations
Review

The Interplay of Host Immunity, Environment and the Risk of Bacterial Vaginosis and Associated Reproductive Health Outcomes

Kerry Murphy et al. J Infect Dis. .

Abstract

Bacterial vaginosis (BV) is one of the most common causes of vaginal symptoms in US women, but its causal mechanism has not yet been defined. BV is more prevalent in women who are immunosuppressed, and several risk factors for the development of BV are associated with lower quantities of immune mediators in vaginal fluid. In contrast, the poor reproductive health outcomes associated with BV, such as preterm birth and human immunodeficiency virus type 1 acquisition, are associated with increased levels of proinflammatory immune mediators in the genital tract. In this article, we discuss how variations in the host immune profile and environmental effects on host immunity may influence the risk of BV, as well as the risk of complications associated with BV.

Keywords: bacterial vaginosis; mucosal immunity; vaginal microbiota.

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Figures

Figure 1.
Figure 1.
Genetic and environmental factors influence mucosal immunity in the reproductive tract. Factors associated with an increased risk for bacterial vaginosis (BV) are also associated with decreased levels of inflammatory immune markers in cervicovaginal secretions, while factors associated with a decreased risk for BV are associated with increased levels. Abbreviations: CRH, corticotropin-releasing hormone; HSV, herpes simplex virus; IFN, interferon; IL, interleukin; NK, natural killer; SNP, single-nucleotide polymorphism; TLR, Toll-like receptor.
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