Ulcerative colitis as a polymicrobial infection characterized by sustained broken mucus barrier

Abstract

To reduce medication for patients with ulcerative colitis (UC), we need to establish the etiology of UC. The intestinal microbiota of patients with inflammatory bowel disease (IBD) has been shown to differ from that of healthy controls and abundant data indicate that it changes in both composition and localization. Small intestinal bacterial overgrowth is significantly higher in IBD patients compared with controls. Probiotics have been investigated for their capacity to reduce the severity of UC. The luminal surfaces of the gastrointestinal tract are covered by a mucus layer. This normally acts as a barrier that does not allow bacteria to reach the epithelial cells and thus limits the direct contact between the host and the bacteria. The mucus layer in the colon comprises an inner layer that is firmly adherent to the intestinal mucosa, and an outer layer that can be washed off with minimal rinsing. Some bacteria can dissolve the protective inner mucus layer. Defects in renewal and formation of the inner mucus layer allow bacteria to reach the epithelium and have implications for the causes of colitis. In this review, important elements of UC pathology are thought to be the intestinal bacteria, gut mucus, and the mucosa-associated immune system.

Keywords: Ulcerative colitis, Mucus, Infection, Bacteria, Etiology

Core tip: Long-term or even life-long medication bothers patients with ulcerative colitis (UC). Existing treatment ignores the cause of UC, so establishing the etiology of UC is the key to resolving this problem. UC can be viewed as a polymicrobial infection that is characterized by a sustained broken mucus barrier with subsequent bacterial migration toward the mucosa and proliferation of complex bacterial biofilms on the epithelial surface. Regulation of mucus secretion and viscosity, suppression of bacterial biofilms, probiotics and immunostimulation should be increasingly considered to treat UC.