In the last decade, the dogma that no bacteria could grow in the acid milieu of the stomach has been destroyed by evidence that the infective agent, H. pylori, is responsible for gastric and duodenal disease. Studies on H. pylori infection suggest that some strains of intestinal bacteria may be responsible for intestinal ulceration and inflammation concomitant with inflammatory bowel diseases (IBD), i.e., ulcerative colitis and Crohn's disease. Evidence for pathophysiological roles for certain strains of luminal bacteria result from a number of IBD animal models. Recent studies on innate immunity, including toll-like receptors and NOD isoforms, suggest that bacterial infections may contribute to intestinal inflammation in genetically susceptible hosts. This brief review focuses on the bacterial pathogenesis and the role of innate immunity in the etiology of IBD's.