Hyperplasia Of Gastric Mucosa Research Articles

Loss of Runx3 function in leukocytes is associated with spontaneously developed colitis and gastric mucosal hyperplasia

RUNX transcription factors are key regulators of lineage-specific gene expression and might be involved in autoimmune diseases. Runx3 plays a role during the development of sensory neurons and T cells and regulates transforming growth factor beta (TGF-beta) signaling in dendritic cells. Here, we report that at 4 weeks of age, Runx3 knockout (KO) mice spontaneously develop inflammatory bowel disease (IBD) characterized by leukocyte infiltration, mucosal hyperplasia, formation of lymphoid clusters, and increased production of IgA. Additionally, at a considerably older age (8 months), the KO mice also develop progressive hyperplasia of the gastric mucosa associated with disturbed epithelial differentiation and cellular hyaline degeneration. Analysis of cytokines in the colonic mucosa of Runx3 KO mice revealed a mixed T helper 1/T helper 2 response. By using immunohistochemistry and RNA in situ hybridization, Runx3 expression in the gastrointestinal tract is detected in lymphoid and myeloid populations but not in the epithelium. The data indicate that loss of leukocytic cell-autonomous function of Runx3 results in IBD and gastric lesion in the KO mice. IBD in humans is viewed as a complex genetic disorder. Several susceptibility loci were identified on different human chromosomes including the chromosomal region 1p36 where RUNX3 resides. It is thus tempting to speculate that mutations in RUNX3 may constitute an IBD risk factor in humans.

Chronic Ihhalation Toxicity and Carcinogenicity Studies of 3-Chloro-2-methylpropene in BDF1 Mice.

Chronic toxicity and carcinogenicity studies of 3-chloro-2-methylpropene (CMP), which has been widely used as an insecticide and chemical intermediate, were carried out in BDF1 mice. CMP was administered to mice in groups of 50 male and 50 female mice by the inhalation route 5 days per week for 104 weeks at doses of 0, 50, 100 or 200 ppm. Male and female mice in the CMP-exposed groups had decreased body weight but no noticeable clinical signs when compared with the control group. Dose-related increases in the incidences of gastric mucosal hyperplasia and squamous cell papilloma were observed in both sexes, and squamous cell carcinoma was observed in only one male mouse in the 100 ppm group. An increased incidence of Harderian gland adenoma in female mice was also recognized. In the nasal cavity, eosinophilic exudate associated with atrophy of olfactory epithelia, respiratory metaplasia of olfactory epithelia and olfactory gland, and eosinophilic changes in respiratory and olfactory epithelia were increased in both sexes.

Cellular Immune Responses Are Essential for the Development of Helicobacter felis-Associated Gastric Pathology

Abstract The bacteria Helicobacter pylori is a major human pathogen that infects over half of the world’s population. Infection initiates a series of changes in the gastric mucosa, beginning with atrophic gastritis and leading in some patients to peptic ulcer disease, mucosa-associated lymphomas, and gastric adenocarcinoma. Although this cascade of events clearly occurs, little is known about the role of the host immune response in disease progression. We have utilized the C57BL/6 Helicobacter felis mouse model to critically analyze the role of the adaptive immune response in the development of Helicobacter-associated gastric pathology. Infection of B and T cell-deficient RAG-1−/− mice or T cell-deficient TCRβδ−/− mice with H. felis resulted in high levels of colonization, but no detectable gastric pathology. Conversely, infection of B cell-deficient μMT mice resulted in severe gastric alterations identical with those seen in immunocompetent C57BL/6-infected mice, including gastric mucosal hyperplasia and intestinal metaplasia. These results demonstrate that the host T cell response is a critical mediator of Helicobacter-associated gastric pathology, and that B cells and their secreted Abs are not the effectors of the immune-mediated gastric pathology seen after H. felis infection. These results indicate that in addition to specific Helicobacter virulence factors, the host immune response is an important determinant of Helicobacter-associated disease.

Hyperplasia of gastric mucosa in donor rats orally infected with Taenia taeniaeformis eggs and in recipient rats surgically implanted with the larvae in the abdominal cavity.

Rats heavily infected with Taenia taeniaeformis larvae in the liver show a remarkable increase in their stomach weight, hyperplasia, and hypergastrinemia. However, it is unknown what causes these phenomena. Hence, as a preliminary study to investigate the importance of larval parasitism in the liver, two experiments were done. In the first experiment, 14 donor rats were orally inoculated with 3,000 T. taeniaeformis eggs. In the second experiment, 136-300 of the larvae obtained from the rats were surgically implanted into the abdominal cavity of 7 recipient rats. Gastrin levels and histopathological changes in the gastric mucosa were investigated. In all, 11 donor rats showed hypergastrinemia and hyperplasia, 5 recipient rats showed gastric mucosal hyperplasia accompanied by excessive mucous cell proliferation, and 2 recipient rats showed hypergastrinemia. These results suggest that parasitism of the liver by the larvae is not essential for the development of hyperplasia and that factors from the larvae might cause these phenomena.

Histopathology and physiopathology of gastric mucous hyperplasia in rats heavily infected with Taenia taeniaeformis.

Rats heavily infected with larval Taenia taeniaeformis show hyperplasia of the gastric mucosa accompanied by mucous cell proliferation, increase in the level of intragastric pH and hypergastrinemia. Sixty one rats were divided into 2 groups designed as infected (36 rats) and control (25 rats) group. These rats were examined with time course of the infection histopathologically and physiopathologically, during 14-112 days postinfection (DPI). In the infected rats, gastric mucosal hyperplasia began to be observed at 56 DPI, and the structural disturbance of zymogenic units in the corpus and mucous units in the antrum had increased with time. However, the degree of these changes in the antrum was weaker than those in the corpus. Alcianblue and/or PAS-positive cells increased in their numbers with time, and 4 types of cells other than typical surface mucous cell and mucous neck cell were observed by electron-microscopy. However, zymogenic and parietal cells decreased in their number after 56 DPI. Further, the infected rats showed changes in the serum concentration of alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, glucose and total protein. Some similarities with Menetrier's disease were discussed.

Hyperplasia of gastric mucosa in rat with peritoneal implantation of Taenia taeniaeformis larvae

Hyperplasia of gastric mucosa in rat with peritoneal implantation of Taenia taeniaeformis larvae

Radiologic features of gastric outlet obstruction in infants after long-term prostaglandin administration.

Long-term prostaglandin (PG) therapy has recently been associated with gastric mucosal hyperplasia. We reviewed the clinical and radiologic (especially sonographic) records of eight patients with complex congenital heart disease who were on PG therapy. Feeding problems, vomiting, and abdominal distension were present in six patients. Barium meal revealed antral narrowing in three patients, suggestive of hypertrophic pyloric stenosis in two. Sonography showed a variable degree of increased gastric mucosal lobulation often accompanied by a marked polypoid or lobular appearance. Cortical hyperostosis related to PG therapy was seen in three patients. PG-associated gastric mucosal hyperplasia can cause feeding problems and pronounced gastric lobulation.

Marked Gastric Mucosal Hyperplasia without Definite Peptic Ulceration Related to a Multifocal Hepatic Gastrinoma

Marked Gastric Mucosal Hyperplasia without Definite Peptic Ulceration Related to a Multifocal Hepatic Gastrinoma

Epizootic Gastritis Associated with Gastric Spiral Bacilli in Cheetahs (Acinonyx jubatus)

An outbreak of vomiting in a group of captive cheetahs (Acinonyx jubatus) was investigated, and histologic examination revealed chronic gastritis characterized by infiltration of lymphocytes and numerous plasma cells and epithelial erosions. Lymphoid follicles, globule leukocytes, scattered neutrophils, and (in one animal) abscessed gastric glands were inconsistent findings. In addition, necropsy of three cheetahs revealed gastric mucosal hyperplasia. Two kinds of bacteria were identified in the stomachs of infected cheetahs. Numerous long, tightly coiled motile Gastrospirillum-like organisms were seen in gastric mucus and in Warthin-Starry-stained sections of mucosa. These bacteria could not be cultured but were transmitted to conventional mice in homogenates of gastric mucosa from infected cheetahs. Ultrastructural examination revealed helical filaments on some of these bacteria. In addition, a smaller Helicobacter sp. was isolated. This organism could be cultured in vitro under microaerophilic conditions. One or both of these bacterial species was probably responsible for the gastritis in these cheetahs.

The gastrin/CCKB antagonist L-365,260 inhibits gastric mucosal cell hyperplasia resulting from acid suppression by loxtidine

The gastrin/CCKB antagonist L-365,260 inhibits gastric mucosal cell hyperplasia resulting from acid suppression by loxtidine

Influence of Long-Term 16,16-Dimethyl Prostaglandin E2 Treatment on the Rat Gastrointestinal Mucosa

We performed acid secretory and histomorphometric studies in rats treated intragastrically with a regimen of 100 micrograms/kg or 5 micrograms/kg of 16,16-dimethyl prostaglandin E2, or of saline every 8 h for 21 days. All animals given the high-dose treatment developed a macroscopically visible enlargement of the ridge at the corpus-forestomach border, due to an increase in connective tissue and epithelial cell layer. Mucosal thickness was significantly increased in all parts of the stomach, the duodenum, and the proximal colon, but most markedly in the gastric antrum (+115%), where it was accompanied by a higher mitotic rate and hyperplasia of surface and foveolar mucous cells. Within the oxyntic area (corpus), high-dose prostaglandin treatment led to an increase in the number of surface and foveolar mucous cells and chief cells. In contrast, both the number of parietal cells and maximal acid output were not influenced. It is unlikely that the hyperplasia of gastric mucosa is mediated by gastrin since gastrin has no trophic effects on the rat antrum and disproportionally increases the parietal cell number of the oxyntic gastric glands.

Biological effects of polychlorinated biphenyls and triphenyls on the subhuman primate

Rhesus monkeys were fed diets containing 300 ppm of a polychlorinated biphenyl (Aroclor 1248) or 5000 ppm of a polychlorinated triphenyl (Aroclor 5460) for 90 days. Both groups of animals developed alopecia, acneform lesions of the skin, subcutaneous edema, liver hypertrophy, and gastric mucosal hypertrophy and hyperplasia. Enlargement of the liver was associated with cell hypertrophy, proliferation of the endoplasmic reticulum, and an increased activity of certain microsomal enzymes.

Polychlorinated biphenyl- and triphenyl-induced gastric mucosal hyperplasia in primates.

Polychlorinated biphenyl or triphenyl ingestion by subhuman primates for 3 months produced hyperplasia and dysplasia of the gastric mucosa. The concentration of the biphenyl within the experimental diet was less than an order of magnitude greater than that occurring in random food samples sold in the United States and less than levels which have occurred in food products as a result of industrial accidents. The increased cellularity, abnormal dysplastic growth pattern, and invasion of the adjacent tissue region indicate compromised gastric function and are suggestive of an eventual neoplastic transformation.