Tu1700 Increased Abundance of Bacteria Producing Hydrogen Sulfide in the Colonic Mucosa of Patients With Ulcerative Colitis and Crohn's Disease

Background: Inflammatory bowel diseases (IBD) include Crohn disease and ulcerative colitis, which have become highly prevalent in developed countries around the world. The peak incidence of the disorders is in young adulthood. While the etiology of IBD is not known, an environmentally triggered exaggerated immune response against the intestinal microbiome is thought to mediate the diseases. The rapid emergence of IBD in the past decades has directed attention towards the potential dietary origins of the disease group. We examined how prenatal nutritional programming may impact predilection towards IBD in a murine model. Methods: C57Bl/6J mice were used. Dams were on control or methyl donor micronutrient (MD) supplemented diets. Offspring were cross-fostered between these dams and subsequently weaned to a control diet. At 90 days of life (young adulthood) chemical colitis was induced by dextran sulfate sodium (DSS). Colonic mucosal Ppar-alpha (Ppara) expression was examined with real time RT-PCR in DSS Naive cross-fostered mice. Colonic mucosal and cecal content microbiomes were interrogated with 454 based pyrosequencing of the 16S rRNA gene. The microbiome changes were tested functionally by colonizing germ free Swiss-Webster mice and exposing those to DSS colitis. Results: Prenatal MD supplementation was sufficient to modulate mucosal Ppara expression and worsen acute colitis in young adulthood. The prenatal dietary intervention induced the postnatal nurturing of a colitogenic microbiome. Conclusions: This is the first study to conclusively show that prenatal nutritional programming can modulate the mammalian host to harbor a colitogenic microbiome. These findings may be relevant for the nutritional developmental origins of IBD