Escherichia coli-derived enterobactin is associated with delayed gut microbiome maturation in infants born to mothers with obesity.

Maternal obesity has been increasingly recognized as a factor influencing early-life microbiome development. However, its impact on the infant gut resistome and virulome remains insufficiently characterized. In this prospective longitudinal study, we investigated gut microbiome composition, antibiotic resistance genes (ARGs), and virulence factor profiles in infants born to mothers with obesity and normal weight during the first year of life. Shotgun metagenomic sequencing was performed on maternal and infant fecal samples collected at birth and at 1, 3, 6, and 12 months. Infants born to obese mothers exhibited delayed microbiome maturation characterized by early enrichment of Pseudomonadota, particularly Escherichia coli and Klebsiella pneumoniae, and reduced abundance of Bifidobacterium species. This compositional pattern was accompanied by a significantly higher ARG burden in early life, including enrichment of genes associated with antibiotic inactivation, efflux mechanisms, and β-lactam resistance. Although taxonomic differences between groups were no longer statistically detectable at the 12-month time point, where the sample size was smallest, functional disparities in the resistome persisted. Additionally, infants born to obese mothers demonstrated increased relative abundance of secretory virulence-associated genes and E. coli-derived enterobactin, suggesting enhanced iron-scavenging capacity and competitive potential of Enterobacteriaceae. Together, these findings suggest that maternal obesity is associated with altered early microbial ecological dynamics, promotes resistome expansion, and may delay transition toward a stable Bacteroidota- and Bacillota-dominated microbiome.IMPORTANCEThe first year of life is a critical window for gut microbiome development, during which early microbial disturbances may influence later health. This study shows that maternal obesity is associated not only with altered infant microbial succession but also with functional changes in the infant gut microbiome, including greater antibiotic resistance gene burden and enrichment of virulence-associated traits. The finding of increased Escherichia coli-derived enterobactin suggests that iron-scavenging mechanisms may help Enterobacteriaceae persist during early infancy and may contribute to delayed microbial maturation. By linking maternal obesity with infant microbiome development, resistome expansion, and virulence-related functions, this work provides new insight into how maternal metabolic status may shape early microbial ecology and potential microbiome-associated risks.