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Colonic Expression of MUC2, MUC5AC, and TFF1 in Inflammatory Bowel Disease in Children

Shaoul, Ron*†; Okada, Yoshio‡; Cutz, Ernest§; Marcon, Margaret A.†

Journal of Pediatric Gastroenterology & Nutrition: May 2004 - Volume 38 - Issue 5 - pp 488-493
Original Articles

Background: The quantity and quality of mucins are affected in inflammatory bowel disease (IBD) both because of a reduction in the number of goblet cells and a decrease in the number of sugar residues per oligosaccharide side chain. Alteration in the types of mucins and aberrant location may contribute to the underlying pathology by affecting the mucus barrier function or may instead be a response to inflammation. The authors used the periodic acid-Schiff/Alcian blue stain to distinguish neutral and acidic mucins, and used specific antibodies to the mature goblet cell mucin MUC2, MUC2 core antigen, foveolar cell mucin MUC5AC, and gastric trefoil factor (TFF1), to characterize their presence and distribution in colonic tissue sections from patients with IBD.

Results: Both core and mature MUC2 were expressed in all colonic goblet cells from patients with ulcerative colitis (UC) and Crohn disease and from healthy controls. MUC5AC and TFF1, which are not normally expressed by colonic tissue, also were expressed in scattered goblet cells, coexpressing with MUC2. In areas of goblet cell depletion, MUC2 was present in cytoplasmic granules of flattened, cuboidal, nongoblet-cell–like surface cells. The staining was more intense and homogenous with the MUC2 core antibody, suggesting expression of relatively immature mucin. Some of these cells also coexpressed MUC5AC but to a lesser extent. These findings are not unique to IBD but were also found in other types of intestinal inflammation.

Conclusion: The study confirms earlier observations that MUC2 is the major colonic mucin in IBD. It appears in two forms: mature MUC2 in goblet cells and immature MUC2 especially in secretory granules of cells that are not phenotypically goblet cells. MUC5AC and TFF1 expression in goblet cells is common in IBD and other inflammatory conditions of the colon. These changes may represent a nonspecific repair function of the colon cells to compensate for damage to barrier function.

*Department of Pediatrics, Bnai Zion Medical Center, Faculty of Medicine, Technion—Israel Institute of Technology, Haifa, Israel; †Division of Gastroenterology and Nutrition, §Hospital for Sick Children, Departments of Pediatrics and Pathology, University of Toronto, Toronto, Ontario, Canada; ‡Department of Nutritional Science, Faculty of Health and Welfare Science Okayama Perfectural University, Soja, Okayama, Japan

Received July 7, 2003; accepted December 31, 2003.

Address correspondence and reprint requests to Dr. Ron Shaoul, Head, Pediatric Day Care Unit, Department of Pediatrics, Bnai Zion Medical Centre, 47 Golomb Street, Haifa 31048, Israel (e-mail: shaoul_r@012.net.il).

Dr. Shaoul was a Canadian Cystic Fibrosis Foundation Research Fellow. He was also supported by grants from the American Physicians Fellowship for Medicine in Israel program, Janssen/Ortho Inc., and the Postgraduate Dyson Fellowship Award from the University of Toronto.

© 2004 Lippincott Williams & Wilkins, Inc.