Maternal prenatal stress is associated with the infant intestinal microbiota.

Maternal prenatal stress has been often associated with infant physical development and health, as well as psychological functioning and behavior. However, the mechanisms underlying these relations remain elusive. The goal of the present study was to prospectively investigate the development of the intestinal microbiota as a potential pathway linking maternal prenatal stress and infant health. The development of the infant intestinal microbiota was followed over the first 110 days after birth in a healthy cohort of 56 vaginally born Dutch infants. Additionally, the relation between infant intestinal microbiota and gastrointestinal and allergic symptoms was examined. Results showed that maternal prenatal stress, i.e., either reported stress or elevated basal maternal salivary cortisol concentrations or both, was strongly and persistently associated with the infants' microbiota composition as determined by a phylogenetic microarray. Infants of mothers with high cumulative stress (i.e., high reported stress and high cortisol concentrations) during pregnancy had significantly higher relative abundances of Proteobacterial groups known to contain pathogens (related to Escherichia, Serratia, and Enterobacter), and lower relative abundances of lactic acid bacteria (i.e., Lactobacillus, Lactoccus, Aerococcus) and Bifidobacteria, altogether characteristics of a potentially increased level of inflammation. Furthermore, this aberrant colonization pattern was related to more maternally reported infant gastrointestinal symptoms and allergic reactions. In conclusion, clear links were found between maternal prenatal stress and the infant intestinal microbiota and health. Although causality cannot be concluded, the results suggest a possible mechanism by which maternal prenatal stress influences the offspring development. These results suggest a potential for bacterial interventions to enhance offspring health and development in pregnant women with stress.