Frontiers in microbiomes · 2026
Altered early-life gut microbiota in offspring of pregnancies complicated by CHD-associated pulmonary hypertension.
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Han Yiyang, Zhang Haofeng, Zhang Jun
Аннотация
BACKGROUND: Pulmonary arterial hypertension is a progressive disease involving the pulmonary vasculature and is defined as a mean pulmonary arterial pressure (mPAP) >20 mmHg at rest. Pulmonary arterial hypertension during pregnancy is associated with increased maternal mortality and adverse fetal outcomes. The present study aimed to investigate differences in the initial meconium microbiota between neonates born to mothers with congenital heart disease-associated pulmonary arterial hypertension (CHD-PAH) and those born to mothers with congenital heart disease (CHD) alone, thereby elucidating the potential influence of pulmonary arterial hypertension on the establishment of the early-life gut microbiome.
METHODS: We collected first-pass meconium samples from neonates in the pulmonary hypertension group (PH group, n = 23) and the control group without pulmonary hypertension (NC group, n = 17) and characterized microbial profiles using 16S rRNA sequencing.
RESULTS: The PH group showed lower alpha diversity, with reduced Shannon and observed features indices (both P < 0.05), whereas Bray-Curtis beta diversity showed substantial overlap between groups. At the phylum level, the overall gut microbial structure was broadly comparable between the PH and NC groups, with no statistically significant differences in the relative abundance of dominant taxa. At the genus level, the mean relative abundance of Streptococcus was significantly lower in the PH group than in the NC group (0.20% vs. 2.09%, P = 0.0072). Predicted functional profiling suggested potential differences in dominant metabolic pathways between groups, including enrichment of ubiquinone biosynthesis and aromatic amino acid/chorismate biosynthesis pathways in the PH group.
CONCLUSION: Collectively, these findings extend current evidence on PAH-related alterations in early-life microbial ecosystems and provide a plausible microbiome-based basis for investigating the biological mechanisms underlying adverse maternal-fetal outcomes associated with pulmonary arterial hypertension.
METHODS: We collected first-pass meconium samples from neonates in the pulmonary hypertension group (PH group, n = 23) and the control group without pulmonary hypertension (NC group, n = 17) and characterized microbial profiles using 16S rRNA sequencing.
RESULTS: The PH group showed lower alpha diversity, with reduced Shannon and observed features indices (both P < 0.05), whereas Bray-Curtis beta diversity showed substantial overlap between groups. At the phylum level, the overall gut microbial structure was broadly comparable between the PH and NC groups, with no statistically significant differences in the relative abundance of dominant taxa. At the genus level, the mean relative abundance of Streptococcus was significantly lower in the PH group than in the NC group (0.20% vs. 2.09%, P = 0.0072). Predicted functional profiling suggested potential differences in dominant metabolic pathways between groups, including enrichment of ubiquinone biosynthesis and aromatic amino acid/chorismate biosynthesis pathways in the PH group.
CONCLUSION: Collectively, these findings extend current evidence on PAH-related alterations in early-life microbial ecosystems and provide a plausible microbiome-based basis for investigating the biological mechanisms underlying adverse maternal-fetal outcomes associated with pulmonary arterial hypertension.