Structural-functional modulation of mucin secretory patterns in the gastrointestinal tract.

1. Mucus-producing cells are clearly identifiable sub-populations of cells in many of the epithelial transport model systems studied, i.e., gastric, jejunal, and colonic epithelia of the rat. 2. The distribution of these cells varies from a predominant location on the mucosal surface of the stomach to a regular degree of interspersion among the dominant columnar epithelial cell population in the small and large intestine. 3. The functional state of these cells can be assessed by a variety of morphological techniques and their biochemical synthetic and secretory capacity estimated by isotopic tracer procedures. 4. In the gastric or jejunal acute ulceration model, sulfomucin production is decreased by aspirin and markedly enhanced by Prostaglandin E1, providing additional evidence for the cytoprotective role of the mucin blanket. 5. With chronic feeding of the bile salt sequestrants which provoke colonic mucosal irritation and injury, there is also a stimulated mucin output. 6. Disruption of the cytoskeletal framework of the mucosal cells by Cytochalasin B or colchicine depresses mucin production. 7. Many of the compounds currently known to phenomenologically perturb mucus synthesis and/or secretion (Table 7) are utilized as probes in the delineation of electrolyte and water transport processes in these epithelial models. It is of interest to not in this volume that renal epithelial tissue do not appear to possess a significant mucin cell population. The developing concept of an association between mucus secretion and antigenic or immune responses may account for this fact. In several epithelial systems, however, modulation of mucin cell function should be taken into consideration in the construction of transport models.