This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Bacterial vaginosis (BV), the most common reproductive tract infection in pregnant women. It is associated with a 2 to 3 increased risk for delivering a baby early or preterm. Preterm birth is the most significant problem in maternal-child health in the United States. The processes that predispose women to developing BV in pregnancy are not well understood. Established risk factors (sociodemographic variables and certain behaviors) accounting for only a small proportion of its incidence. Reproductive tract infections such as BV produce preterm birth by ascending into the uterus and establishing an infection and inflammation in the uterus. However, not all pregnant women with BV (BV+) deliver preterm. The determinants of increased susceptibility for preterm birth among some but not all BV+ women are not known. The prevalence of BV in pregnancy and infection-associated preterm birth is unevenly distributed in the U.S. population, with the largest disparities occurring along racial/ethnic lines, e.g., African-American women have an approximately 2-fold higher prevalence of BV during pregnancy, and an approximately 4-fold higher incidence of infection-associated early preterm birth than non-Hispanic White women (Goldenberg et al, 1996; Hillier et al, 1995; Meis et al, 1995; Royce et al, 1999). The underlying causes of these racial/ethnic disparities in the prevalence and adverse consequences of infection in pregnancy are largely unexplained. Many issues remain unanswered about the role of reproductive tract infection (bacterial vaginosis) in preterm birth. Two questions of particular interest are, first, what is/are the factor(s) that affect susceptibility to developing BV during pregnancy, and second, based on the findings that not all women with BV during pregnancy deliver prematurely, what are the factors that affect susceptibility to preterm birth in the presence of BV (Romero et al, 2001)? We have hypothesized that stress and stress biology may play an important role in increasing susceptibility for developing BV in pregnancy. We previously have found, in a sample of 454 pregnant women assessed at 14 weeks gestation, that high levels of chronic maternal psychosocial stress were associated with a 2.2-fold increase in BV prevalence after adjusting for the effects of established risk factors (Culhane et al, 2001). The objective of the present proposal is to examine the relationship between stress physiology and immune function in the development of BV, and the effect of stress on susceptibility to preterm birth among BV+ women. We postulate that prenatal stress a) increases the susceptibility for acquiring BV, and b) increases the adverse consequences of established BV. We focus on the endocrine and immune systems as the primary biological processes of interest because both systems a) are highly responsive to stress, b) regulate susceptibility to developing infection as well as to its negative consequences, and c) participate in the physiology and pathophysiology of term and preterm parturition, respectively.
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