The inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, are T cell-mediated diseases that are characterized by chronic, relapsing inflammation of the intestinal tract. The pathogenesis of IBD involves the complex interaction between the intestinal microflora, host genetic and immune factors, and environmental stimuli. Epidemiological analyses have implicated acute bacterial enteritis as one of the factors that may incite or exacerbate IBD in susceptible individuals. In this review, we examine how interactions between the common enteric pathogen Campylobacter jejuni (C. jejuni), the host intestinal epithelium, and resident intestinal microflora may contribute to the pathogenesis of IBD. Recent experimental evidence indicates that C. jejuni may permit the translocation of normal, noninvasive microflora via novel processes that implicate epithelial lipid rafts. This breach in intestinal barrier function may, in turn, prime the intestine for chronic inflammatory responses in susceptible individuals. Insights into the interactions between enteric pathogens, the host epithelia, and intestinal microflora will improve our understanding of disease processes that may initiate and/or exacerbate intestinal inflammation in patients with IBD and provide impetus for the development of new therapeutic approaches for the treatment of IBD.