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MUC2 is the primary component of the mucin barrier that separates the intestinal microbiota and the intestinal epithelium. This mucous barrier is affected by both luminal/microbial factors and host/immune factors, both of which have genetic and environmental determinants. The complex interactions between these players in health and disease states are not fully understood. Inflammatory bowel disease (IBD) has both genetic and environmental etiologies that lead to the breakdown of the epithelial barrier. In this review, we explore the up-to-date evidence that implicates mucin in the pathogenesis of IBD. In IBD, quantitative changes in mucin secretion occur, as well as structural changes in mucin's glycoprotein core and the sulfation and sialylation of mucin's oligosaccharide residues. These changes are associated with a diminished functionality of the mucous barrier. We identify the various genetic mutations associated with these changes and outline the animal models that have enhanced the current understanding of the genetic basis for IBD. Further study is needed to better characterize the immune and genetic influences on mucin expression and secretion and role of endoplasmic reticulum stress and a defective unfolded protein response in mediating these changes.

Objective: JC virus (JCV) is thought to infect approximately 80% of the human population. Antibodies against JCV can be found in the sera of many people with and without colorectal carcinoma (CRC). We hypothesized that JCV antibody titer will be higher in CRC patients than in healthy controls. Aim: To evaluate this hypothesis in a cohort of patients undergoing colonoscopy. We compared JCV antibody titers in patients with simple adenoma, advanced adenomatous polyp (AAP), CRC, and healthy controls, and evaluated JCV DNA in the tissue. Methods: Ninety-seven patients undergoing colonoscopy offered to participate in the study. Normal colonoscopy, simple adenoma, AAP, and CRC were found in 41, 19, 12, and 25 cases, respectively. A blood sample was taken for JCV DNA isolation and serology. In 18 patients with CRC or AAP tissue samples were taken for JCV DNA isolation and T-antigen (T-Ag) detection. Results: A positive correlation was found between a JCV antibody titer and advanced colonic pathology. The average titer for normal controls, simple polyp, AAP, and CRC was 2.61 ± 0.72, 2.95 ± 0.77, 3.33 ± 0.76, and 3.30 ± 0.50 log, respectively (P < 0.001). Viral DNA could not be shown in the serum. The presence of neoplastic tissue T-Ag (in 33.3% of the patients) was not associated with a difference in the log titer of serum antibody. Conclusions: In this study we showed that patients with advanced neoplasia, compared with patients with normal colonoscopy, harbor a higher JCV antibody titer in the serum. If confirmed, our finding may serve as a marker for CRC or for an earlier stage of AAP.