Abstract
Biomechanical and molecular processes of premature cervical remodeling preceding spontaneous preterm birth (sPTB) likely result from interactions between the cervicovaginal microbiota and host immune responses. A non-optimal cervicovaginal microbiota confers increased risk of sPTB. The cervicovaginal space is metabolically active in pregancy; microbiota can produce, modify, and degrade metabolites within this ecosystem. We establish that cervicovaginal metabolomic output clusters by microbial community in pregnancy among Black individuals, revealing increased metabolism within the amino acid and dipeptide pathways as hallmarks of a non-optimal microbiota. Few differences were detected in metabolomic profiles when stratified by birth outcome. The study raises the possibility that metabolites could distinguish women with greater risk of sPTB among those with similar cervicovaginal microbiota, and that metabolites within the amino acid and carbohydrate pathways may play a role in this distinction.
Highlights
Biomechanical and molecular processes of premature cervical remodeling preceding spontaneous preterm birth likely result from interactions between the cervicovaginal microbiota and host immune responses
We reported outcomes from a 2000-women cohort revealing that community state types (CST) IV, specific bacterial taxa, and local immune factors were significantly associated with s PTB9
Differences in gestational age are noted between spontaneous preterm birth (sPTB) and term pregnancies (p-value < 0.001), as expected based on study design but not between women classified as having CST I or CST IV vaginal microbiomes (p = 0.52)
Summary
Biomechanical and molecular processes of premature cervical remodeling preceding spontaneous preterm birth (sPTB) likely result from interactions between the cervicovaginal microbiota and host immune responses. We establish that cervicovaginal metabolomic output clusters by microbial community in pregnancy among Black individuals, revealing increased metabolism within the amino acid and dipeptide pathways as hallmarks of a non-optimal microbiota. Not all cases of sPTB occur in the setting of a non-optimal microbiota These collective observations raise questions about other undefined factors in the cervicovaginal space that might mediate or distinguish clinical outcome in the presence of the same microbiota. Our group previously identified a cervicovaginal metabolomic signature in pregnancy, including distinct biochemicals associated with sPTB29, 30 While these early studies suggest that metabolites may provide a lens into mechanisms underlying premature cervical remodeling, they did not incorporate data on microbiota composition. No study in pregnancy to date has examined the cervicovaginal metabolome within the same ethnic group and microbial community to determine microbiome-metabolome patterns that may identify women at greatest risk for sPTB
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