PROBLEM Spontaneous labor at term involves leukocyte recruitment and infiltration into the choriodecidua; yet, characterization of these leukocytes and their immunological mediators is incomplete. The purpose of this study was to characterize the immunophenotype of choriodecidual leukocytes as well as the expression of inflammatory mediators in human spontaneous parturition at term. METHOD OF STUDY Choriodecidual leukocytes were analyzed by FACS, immunohistochemistry, and RT-PCR in three different groups: (i) preterm gestation delivered for medical indications without labor; (ii) term pregnancy without labor; and (iii) term pregnancy after spontaneous labor. RESULTS Two T-cell subsets of memory-like T cells (CD3+CD4+CD45RO+ and CD3+CD4−CD8−CD45RO+ cells) were identified in the choriodecidua of women who had spontaneous labor. Evidence for an extensive immune signaling network composed of chemokines (CXCL8 and CXCL10), chemokine receptors (CXCR1-3), cytokines (IL-1β and TNF-α), cell adhesion molecules, and MMP-9 was identified in these cells during spontaneous labor at term. CONCLUSIONS The influx of memory-like T cells in the choriodecidua and the evidence that they are active by producing chemokines and cytokines, and expressing chemokine receptors, cell adhesion molecules, and a matrix-degrading enzyme provides support for the participation of the adaptive immune system in the mechanisms of spontaneous parturition at term.

Preterm birth is a public health issue of global significance, which may result in mortality during the perinatal period or may lead to major health and financial consequences due to lifelong impacts. Even though several risk factors for preterm birth have been identified, prevention efforts have failed to halt the increasing rates of preterm birth. Epidemiological studies have identified air pollution as an emerging potential risk factor for preterm birth. However, many studies were limited by study design and inadequate exposure assessment. Due to the ubiquitous nature of ambient air pollution and the potential public health significance of any role in causing preterm birth, a novel focus investigating possible causal mechanisms influenced by air pollution is therefore a global health priority. We hypothesize that air pollution may act together with other biological factors to induce systemic inflammation and influence the duration of pregnancy. Evaluation and testing of this hypothesis is currently being conducted in a prospective cohort study in Mexico City and will provide an understanding of the pathways that mediate the effects of air pollution on preterm birth. The important public health implication is that crucial steps in this mechanistic pathway can potentially be acted on early in pregnancy to reduce the risk of preterm birth.

Maternal obesity during pregnancy is rising and is associated with increased risk of developing gestational diabetes mellitus (GDM), defined as glucose intolerance first diagnosed in pregnancy (1). Fetal growth is determined by the maternal nutrient supply and placental nutrient transfer capacity. GDM-complicated pregnancies are more likely to be complicated by fetal overgrowth or excess adipose deposition in utero. Infants born from GDM mothers have an increased risk of developing cardiovascular and metabolic disorders later in life. Diverse factors, such as ethnicity, age, fetal sex, clinical treatment for glycemic control, gestational weight gain, and body mass index among others, represent a challenge for studying underlying mechanisms in GDM subjects. Determining the individual roles of glucose intolerance, obesity, and other factors on placental function and fetal growth remains a challenge. This review provides an overview of changes in placental macronutrient transport observed in human pregnancies complicated by GDM. Improved knowledge and understanding of the alterations in placenta function that lead to pathological fetal growth will allow for development of new therapeutic interventions and treatments to improve pregnancy outcomes and lifelong health for the mother and her children.

Although the isolated effects of several specific nutrients have been examined, little is known about the relationship between overall maternal diet during pregnancy and fetal development and growth. This study evaluates the association between maternal diet and low birthweight (LBW) in 660 pregnant women from the Pregnancy Research on Inflammation, Nutrition,& City Environment: Systematic Analyses (PRINCESA) cohort in Mexico City. Using prior day dietary intake reported at multiple prenatal visits, diet was assessed prospectively using a priori (Maternal Diet Quality Score [MDQS]) and a posteriori (dietary patterns extracted by factor analysis) approaches. The association between maternal diet and LBW was investigated by logistic regression, controlling for confounders. Adherence to recommended guidelines (higher MDQS) was associated with a reduced risk of LBW (OR, 0.22; 95% confidence interval [0.06, 0.75], P < .05, N = 49) compared with the lowest adherence category (reference group), controlling for maternal age, education, height, marital status, pre‐pregnancy body mass index, parity, energy intake, gestational weight gain, and preterm versus term birth; a posteriori dietary patterns were not associated with LBW risk. Higher adherence to MDQS was associated with a lower risk of having an LBW baby in this sample. Our results support the role of advocating a healthy overall diet, versus individual foods or nutrients, in preventing LBW.