Three-dimensional structure of the rat intestinal wall (Mucosa and submucosa).

A novel population of subepithelial platelet-derived growth factor receptor α-positive cells in the mouse and human colon

“…This overlapping organization might be equivalent to the double layers of subepithelial PDGFR␣ ϩ cells and subepithelial myofibroblasts we noted in human and murine colonic mucosae. The distribution of subepithelial PDGFR␣ ϩ cells is somewhat similar to the distribution of fibroblast-like cells reported in a previous ultrastructural study of rat colonic mucosa (30). We found that subepithelial myofibroblasts merged into the muscularis mucosa, and their distribution appeared to be less organized at the bottoms of crypts and did not extend to the luminal surface of the epithelium (Figs.…”

Polarized Uterine Epithelial Cells Preferentially Present Antigen at the Basolateral Surface: Role of Stromal Cells in Regulating Class II-Mediated Epithelial Cell Antigen Presentation

“…Of equal importance was the identification of protrusions from the basal parts of epithelial cells that passed through these fenestrations into the lamina propria to make physical contact with underlying immune cells. In other studies, they demonstrated the penetration of the epithelial processes and close contact between lymphocytes and so forth and the epithelial cells (59). Our finding that polarized epithelial cells present Ags to T cells placed in contact with the basolateral surface suggest that the anatomical associations seen by Komuro represent a intercellular communication between these different cell types.…”

PAR1-dependent and independent increases in COX-2 and PGE2 in human colonic myofibroblasts stimulated by thrombin

“…In these circumstances, the luminal bacteria and their products (as mimicked by LPS) induce an inflammatory response that includes increased vascular permeability (15,30). Because the myofibroblast is closely associated with the capillary network of intestinal villi (29), elevations in mucosal levels of thrombin resulting from vascular leakage will, according to our data, increase COX-2-derived PGE 2 release from the myofibroblast and thereby induce epithelial chloride secretion. This action of thrombin, therefore, represents an important host defense mechanism.…”