These results strongly suggest that both pathogenic and commensal bacteria contribute to the disease and mortality suffered by Muc2−/− mice, since A/E bacterial infection-induced disruption of the epithelial barrier allows massive translocation of both pathogenic and commensal bacteria out of the intestinal lumen and into mucosal tissues, and pathogens into systemic compartments, leading to bacteremia. This evidence concerns the gene MUC2 and bacterial infectious disease with sepsis.