H1N1 infection during pregnancy elicits changes in the intestinal epithelial barrier, intestinal microbiome, and immune microenvironment 4386

Abstract Description Influenza A virus infections during pregnancy are associated with increased risk of hospital admission and adverse perinatal and fetal outcomes. 2009 H1N1 infection of outbred pregnant mice results in increased maternal morbidity, fetal growth restriction, and developmental delays in offspring. The maternal gut microbiome is essential in maintaining homeostasis during pregnancy, and its disruption can restrict placental growth and impair feto-placental vascularization, resulting in smaller offspring. Utilizing our model of maternal H1N1 infection, we characterized the fecal microbiome and its relation to intestinal barrier permeability and inflammation. H1N1-infected dams displayed distinct microbial community composition and reduced diversity compared to mock controls. H1N1-infected dams exhibited significantly higher relative abundances of Muribaculum spp., a mucus-degrading bacterium associated with ulcerative colitis models. H1N1-infected dams also had more endotoxin in the serum, suggesting increased intestinal barrier permeability. When examining the intestinal immune phenotype, maternal H1N1 infection resulted in increased proportions of gd T cells and macrophages along with increased concentrations of diverse cytokines associated with inflammatory bowel disease and colitis in mice. Examining H1N1-induced changes in distal mucosal sites during infection may guide the development of novel therapeutic strategies to improve maternal and child health. Funding Sources T32AI138953 and BAA 75N93021C00045 Topic Categories Viral Immunology (VIR)