Mucins are high-molecular-weight glycoproteins that form the main structural component of the mucus covering epithelial surfaces in the gastrointestinal, respiratory, and urogenital tracts. They support epithelial integrity by protecting against microbial invasion, dehydration, and mechanical or chemical insults, while facilitating the transit of luminal contents. Beyond their structural function, mucins play key roles in molecular recognition. Their extensive glycosylation enables interactions with a wide range of molecules and allows the discrimination between pathogenic and commensal microorganisms at mucosal surfaces. Mucins help maintain mucosal homeostasis by preventing pathogen adhesion and colonization, while simultaneously providing nutrients to commensal species, supporting their stability, and maintaining spatial segregation from epithelial surfaces. Aberrant expression of mucin subtypes or alterations in their glycosylation patterns are associated with numerous diseases, including a wide spectrum of cancers and inflammatory disorders. The immunological relevance of the esophageal mucosa has only recently been recognized. Advances in the study of the esophageal mucosa-associated immune surveillance system and its interactions with structural components of this organ’s surface, including mucins, have shed light on unique pathological processes in the esophagus, such as Barrett’s esophagus, gastroesophageal reflux disease, and eosinophilic esophagitis. This review focuses on the role of esophageal mucins in inflammation, compiling current evidence to provide an integrated overview of mucin-driven inflammatory mechanisms.
Arias-González et al. (Thu,) studied this question.