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Results for “Paneth Cells”

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At least 325 records · Page 18Linked to original sources
PubMed2001

Mucosal T cells regulate Paneth and intermediate cell numbers in the small intestine of T. spiralis-infected mice.

Secretions of Paneth, intermediate and goblet cells have been implicated in innate intestinal host defense. We have investigated the role of T cells in effecting alterations in small intestinal epithelial cell populations induced by infection with the nematode Trichinella spiralis. Small intestinal tissue sections from euthymic and athymic (nude) mice, and mice with combined deficiency in T-cell receptor beta and delta genes [TCR(beta/delta)-/-] infected orally with T. spiralis larvae, were examined by electron microscopy and after histochemical and lineage-specific immunohistochemical staining. Compared with uninfected controls, Paneth and intermediate cell numbers increased significantly in infected euthymic and nude mice but not infected TCR(beta/delta)-/- mice. Transfer of mesenteric lymph node cells before infection led to an increase in Paneth and intermediate cells in TCR(beta/delta)-/- mice. In infected euthymic mice, Paneth cells and intermediate cells expressed cryptdins (alpha-defensins) but not intestinal trefoil factor (ITF), and goblet cells expressed ITF but not cryptdins. In conclusion, a unique, likely thymic-independent population of mucosal T cells modulates innate small intestinal host defense in mice by increasing the number of Paneth and intermediate cells in response to T. spiralis infection.

Animals↗
PubMed1995

Ultrastructural immunogold localization of subcellular sites of TNF-alpha in colonic Crohn's disease.

Tumor necrosis factor-alpha, a proinflammatory cytokine, might have an important role(s) in initiating, modifying, and/or sustaining chronic inflammatory processes such as those that characterize Crohn's disease, an inflammatory bowel disease of unknown etiology. We used an immunogold ultrastructural morphometric approach to localize tumor necrosis factor-alpha in colonic Crohn's disease biopsies. Tumor necrosis factor-alpha was present in seven cell types (fibroblasts, eosinophils, mast cells, macrophages, colonic epithelial absorptive cells, Paneth cells, neutrophils). Tumor necrosis factor-alpha-containing subcellular organelles included lipid bodies (fibroblasts, eosinophils, macrophages, mast cells, colonic epithelial cells, neutrophils), secretory granules (eosinophils, Paneth cells), phagolysosomes (macrophages, colonic epithelial cells), and Golgi structures and vesicle membranes (neutrophils). A gradient of extracellular tumor necrosis factor-alpha immunoreactivity surrounded eosinophils, mast cells, and macrophages. P values of gold counts/microns2 were significant for all cells, organelles, and extracellular spaces measured, and all positive structures significantly exceeded the background labeling density/microns2. Specificity controls (normal rabbit serum, tumor necrosis factor-alpha-absorbed primary antibody) either failed to label these sites or gave markedly reduced specific tumor necrosis factor-alpha labeling, respectively. These findings represent the first ultrastructural localization of the subcellular sites of TNF-alpha in vivo in seven cell lineages in human colonic tissues.

Adult↗
PubMed1994

Proliferation and differentiation of the small intestinal epithelium: from Petri dish to bedside.

The small intestinal epithelium is a continuously renewing cell system in which two main compartments can be defined: the crypt compartment and the villus compartment. The crypt compartment houses the proliferative cells (stem cells) that give birth to the four types of differentiated enterocytes (absorptive enterocytes, goblet cells, enteroendocrine cells, Paneth cells) that, with the exception of Paneth cells, populate the villus compartment. Enterocyte proliferation, differentiation and migration are regulated by a complex network of cell-cell and cell-matrix information, and modulated by growth factors, luminal factors and, possibly, hormones. The intimate mechanisms underlying the fascinating life of the enterocytes are the object of intensive investigation although insights have come from studies "in vitro" and in transgenic animals. The enormous proliferative potential makes the small bowel an extremely plastic organ, able to adapt to various injuries and adverse conditions and to completely recover even from extensive damage. Knowledge of the biologic mechanisms of adaptation has begun to affect therapeutic approaches to a number of intestinal diseases and the future will see a significant advancement in their management. More important, understanding the molecular mechanisms regulating the perfect equilibrium between proliferation and differentiation of the intestinal enterocytes will eventually help disclose the dark side of cancer.

Cell Cycle↗
PubMed1985

Long-term comparative effect of cholecystokinin and gastrin on mouse stomach, antrum, intestine, and exocrine pancreas.

Mice were injected three times a day for 12 days with 300 micrograms/kg body weight of gastrin G17 or 37.5 Ivy dog U/kg body weight of CCK or saline. Other mice were also injected four times an hr for 1 hr with 7.5 micrograms/kg of gastrin, nine Ivy dog U/kg of CCK or saline; 1 hr before killing, they were injected with tritiated thymidine to evaluate the labelling indices in peptic, antral, duodenal, jejunal, and ileal mucosae. Four hours after the first injection of the two peptides, the peptic labelling indices increased while those of intestinal mucosa increased 8 hr after these injections. Long-term injections of CCK had a trophic effect on secretory cells of the digestive tract: the number of gastric zymogenic cells, Paneth cells, and the mucous cells of Brünner glands were hypertrophied. The pepsin, amylase, chymotrypsin, and lysozyme activities increased in stomach, exocrine pancreas, and intestine, respectively. Neither parietal cells nor intestinal enterocytes and hydrolase activities were affected. The trophic effect of long-term injections of gastrin is confirmed on parietal cells and exocrine pancreatic parenchyma and is demonstrated in Paneth cells. Confirming cytological results, pancreatic lipase and amylase activities and intestinal lysozyme activity were increased after gastrin. Although CCK and gastrin have a structural analogy, these two peptides did not affect the same cellular types. A specific action of CCK on the main secretory cells of the digestive mucosa is demonstrated.

Amylases↗
PubMed1999

Development of dysplastic mucinous epithelium from endometriosis of the appendix.

AIM: We report an unusual case of mucinous metaplasia and epithelial dysplasia occurring in endometriotic epithelium in the appendix. METHODS AND RESULTS: A 39-year-old woman developed an appendiceal endometriosis in which the endometrial glands displayed extensive areas consisting of mucinous epithelium and Paneth cells. Focally the mucinous epithelium showed low-grade epithelial dysplasia. These changes occurred in portions of the endometriotic tissue closest to the appendiceal lumen. Both the intestinal and endometrial epithelial components were surrounded by typical endometrial-type stroma showing positive reactivity for oestrogen receptor. CONCLUSIONS: Formation of the mucinous epithelium most likely represents a metaplastic process of the endometrial epithelium rather than a result of a simple 'collision' of the appendiceal and endometrial epithelium. Further support for this being a metaplastic process was the presence of glandular structures containing a mixture of mucinous cells, goblet cells, Paneth cells, ciliated and nonciliated endometrial cells, and ciliated and nonciliated mucinous cells, all showing the same positive reactivity for oestrogen receptor. The disposition of mucinous epithelium in the foci of endometriosis in this case suggests that the appendiceal mucosa or extracellular mucin may play a role as an inducer of mucinous cell metaplasia in endometriotic epithelium.

Adult↗
PubMed1989

Functional activity of intestinal epithelium demonstrated by mRNA in situ hybridization.

To elucidate the synthetic activity in relation to the morphology of the epithelial cells of the small and large intestine, in situ hybridization with a poly-deoxyribothymidine (poly d(T)) probe was applied to paraffin sections of formalin-fixed blocks. This effectively displays poly-adenylated RNA and, by implication, messenger RNA (mRNA). By minimizing proteinase K pretreatment, the relative concentrations of cellular mRNA were visualized. This revealed minimal mRNA in crypt columnar cells, and maximal mRNA in proliferating cells and in cells showing terminal differentiation. The latter include surface epithelial cells, endocrine cells, Paneth cells, and maturing, but not mature, goblet cells. The goblet cells showing positive hybridization can be regarded as active cells and show characteristic morphology. Such cells are particularly evident in untreated coeliac disease, remitting ulcerative colitis, and transitional mucosa. The proliferating cells showing increased hybridization include normal mitotically active crypt epithelium, regenerating epithelium in ulcerative colitis, adenomatous epithelium, and adenocarcinomatous epithelium. The similarity of hybridization between metaplastic polyp epithelium and surface colonocytes is consistent with the concept that metaplastic polyps are formed of cells showing premature terminal differentiation.

Adenocarcinoma↗