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Mucin 2 (MUC2) is the primary gel-forming glycoprotein of the intestinal mucus layer, synthesized and secreted by goblet cells (UniProt P19835). It forms a complex, hydrated physical barrier that protects the intestinal epithelium from mechanical stress, digestive enzymes, and pathogenic microorganisms (Hansson, 2020). In the large intestine, MUC2 creates a two-layered structure: an inner stratified layer that is largely devoid of bacteria and an outer loose layer that serves as a habitat for the commensal microbiota (Kim & Ho, 2010). This barrier is essential for maintaining intestinal homeostasis and preventing inappropriate immune activation by luminal contents. Dysregulation of MUC2, including reduced expression or altered glycosylation, is a hallmark of inflammatory bowel diseases like ulcerative colitis and is associated with increased susceptibility to infection (Hansson, 2020). Furthermore, changes in MUC2 expression are frequently observed in colorectal cancer, where it can influence tumor progression and metastasis (Kim & Ho, 2010). Therapeutic strategies targeting MUC2 focus on stimulating its production or enhancing its barrier properties to restore mucosal integrity. Drugs like rebamipide are known to stimulate mucin secretion, while others like sucralfate provide a protective coating by interacting with the mucosal surface (Arakawa et al., 2005; Nagashima et al., 1981). Understanding the regulation of MUC2 remains a critical area for developing treatments for chronic gastrointestinal disorders.
Stimulation of mucin synthesis and secretion by goblet cells; physical binding to the mucosal surface to enhance barrier integrity (Arakawa et al., 2005; Nagashima et al., 1981).
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