Vaginal and oral microbes, host genotype and preterm birth

Abstract

Preterm birth (PTB) is a leading cause of infant mortality and morbidity in the U.S. and across the globe. Infection and associated inflammation are important initiators for PTB pathways; an estimated 40% of PTBs are attributed to amniochorionic-decidual or systemic inflammation. Historically, intrauterine infections have been implicated in PTB; recent evidence suggests that infections remote from the fetal site may also be causative. There is strong epidemiological evidence that bacterial vaginosis and periodontitis -- two syndromes characterized by perturbations in the normal vaginal and oral bacterial microflora respectively-- are linked to infection-associated PTB. Oral and vaginal environments are similar in their bacterial microbiology; identical bacterial species have been independently isolated in periodontitis and bacterial vaginosis. Periodontitis and bacterial vaginosis also share many behavioral and sociodemographic risk factors suggesting a possible common pathophysiology. Genetic polymorphisms in host inflammatory responses to infection are shared between bacterial vaginosis, periodontitis and PTB, suggesting common mechanisms through which host genotype modify the effect of abnormal bacterial colonization on preterm birth. We review the state of knowledge regarding the risk of PTB attributable to perturbations in bacterial flora in oral and vaginal sites and the role of host genetics in modifying the risk of infection-related PTB. We posit that bacterial species that are common in perturbed vaginal and oral sites are associated with PTB through their interaction with the host immune system.

Clinical Risk Factors for Preterm Birth

“…Other studies have shown that bacteria, which cause placental infection, are capable of producing prostagandins, which disrupts uterine quiescence, causing cervical softening and preterm birth (Bejar, 1981). In addition, vaginal infection and associated inflammation, causes an inflammatory response with cytokines, which cause a further increase in prostaglandin levels (Srinivasan, et al, 2009). Raised levels of neutrophils and a raised pH of more than 5, was shown to be significantly associated with preterm birth.…”

“…Oral and vaginal sites are comparable in their bacterial microbiology. Mothers with periodontitis and bacterial vaginosis also share similar social and sociodemographic risk factors, suggesting a common pathophysiology (Srinivasan, et al, 2009). …”

Microbiome and women's health (literature review)

“…Результаты мно-гих исследований показали, что микробиом детей, которые родились вагинальным путем, отличается от микробиома детей, рожденных с помощью кесарева сечения. Наблюдения показали, что кесарево сечение повышает риск заражения ребенка некоторыми инфек-циями [10, 24,112].…”

Getting to Know Our Guests: Characterizing the Reproductive Microbiome by Next Generation Sequencing

“…Chlamydia is the main etiological factor responsible for the rise in sexually transmitted disease among the young and infection with this and other pathological organisms including Gonococcus, Ureaplasma, Mycoplasma, Candida, Gardnerella, and Trichomonas provoke immune responses that can lead to inflammatory and frequently permanent damage [Larsen and Hwang 2010]. Moreover, poorly understood changes in the LGT flora associated with vaginosis may be connected to recurrent miscarriage [McGregor and French 2000] and preterm labor has long been thought to have a bacteriological component [Srinivasan et al 2009]. However, our knowledge of the composition and diversity of the healthy LGT's microflora and how it might help protect this special environment from potentially invasive pathogens is still rather poor [Verstraelen et al 2009].…”