Vaginal and oral microbes, host genotype and preterm birth

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