Exploratory evaluation of labor-associated inflammatory profiles in low-risk nulliparous subgroups during induced and spontaneous labor - maternal morbidity and mortality remain a critical public…

The National Institute for Minority Health and Health Disparities awarded Vanderbilt University $217,950 on September 1, 2026, under the Minority Health and Health Disparities Research program (CFDA 93.307) to conduct an exploratory evaluation of labor-associated inflammatory profiles in low-risk nulliparous women during induced and spontaneous labor.

The research investigates physiologic mechanisms underlying racial disparities in cesarean birth rates among nulliparous, term, single, vertex (NTSV) births—a standardized obstetric population. Within this group, cesarean rates are 31.5 percent among Black women compared with 25.9 percent among Hispanic women and 25.5 percent among White women. Failed induction and labor dystocia account for nearly half of NTSV cesareans and occur more frequently in Black women. The study will examine whether chronic inflammatory burden alters physiologic immune activation during labor, testing the hypothesis that chronic, low-grade inflammation disrupts labor through either attenuated immune responsiveness or additive inflammatory signaling that exceeds physiologic thresholds, either of which may impair uterine contractility and labor efficiency.

The award is classified as a Project Grant, an assistance type supporting basic, clinical, social, and behavioral research to reduce health disparities in minority populations. Performance takes place in Nashville, Tennessee, with a period of performance from September 1, 2026, through February 29, 2028.

Exploratory evaluation of labor-associated inflammatory profiles in low-risk nulliparous subgroups during induced and spontaneous labor - maternal morbidity and mortality remain a critical public health challenge in the united states, with black women experiencing disproportionately high rates of adverse maternal outcomes and cesarean birth. Racial disparities in cesarean birth persist among low-risk nulliparous, term, single, vertex (NTSV) births, a standardized population with similar baseline obstetric risk. Within this population, the cesarean rate is 31.5% among black women compared with 25.5% among white women and 25.9% among hispanic women. Failed induction and labor dystocia (slow or arrested labor progress) account for nearly half of NTSV cesareans, and black women experience both more frequently. However, the physiologic mechanisms underlying these conditions remain undefined, and whether chronic inflammatory burden alters physiologic immune activation during labor has never been determined. Labor onset and progression are mediated by acute inflammatory processes that amplify through coordinated positive feedback signaling within the cervix, myometrium, fetal membranes, and maternal circulation. While physiologic inflammation is necessary for efficient labor, dysregulated inflammatory signaling-whether inadequate or excessive-can impair uterine contractility and labor performance, even in the absence of infection. Chronic, low-grade inflammation, a hallmark of many chronic diseases, may alter responsiveness to labor-associated immune activation. We propose that chronic inflammation disrupts physiologic labor through one of two maladaptive pathways: (1) attenuated immune responsiveness to acute labor activation or (2) additive inflammatory signaling exceeding physiologic thresholds. Either pathway may impair uterine contractility and labor efficiency, contributing to failed induction, labor dystocia, and cesarean birth. These mechanisms are biologically relevant to all women but are hypothesized to be most pronounced among those with elevated chronic inflammatory burden. Accordingly, oversampling black NTSV women is a scientifically justified strategy to identify inflammatory trajectories associated with labor inefficiency. We will enroll 120 low-risk NTSV women (60 black, non-hispanic; 60 other, any ethnicity) admitted to vanderbilt university medical center for induction or spontaneous labor. Group-based trajectory modeling will identify latent trajectories of maternal plasma inflammatory biomarkers (IL-1Β, IL-6, IL-8, TNF-Α) across induction, spontaneous early labor, and active labor, and linear mixed-effects models will compare groups to generate preliminary effect size and variance estimates that will refine hypotheses and inform future adequately powered studies. Defining inflammatory trajectories during labor will generate foundational evidence on physiologic mechanisms of labor inefficiency. In the long term, these findings will inform the development of biologically informed approaches for individualized labor assessment and clinical management aimed at reducing preventable cesarean births and improving maternal outcomes.