Early Proliferative Changes in Rat Pyloric Mucosa Induced with N-Methyl-N'-Nitro-N-Nitrosoguanidine(MNNG)1

MX is a strong direct acting mutagen on Salmonella typhimurium TA100 and is present in chlorinated tap water which contains organic compounds. MX was administered orally to 7-week-old male F344 rats, and its geno-toxicity in the pyloric mucosa of stomach was examined by analysis of DNA single strand scissions by the alkaline elution method. The effect of MX on cell proliferation was examined by assays of the inductions of replicative DNA synthesis and ornithine decarboxylase. MX at closes of 20-48 mg/kg body weight induced DNA single strand scissions dose-dependently (p<0.02) in the pyloric mucosa of the stomach 2 h after its administration. Moreover at doses of 10-60 mg/kg body weight, it induced up to 21-fold increase in replicative DNA synthesis (p<0.01) 16 h after its administration. At doses of 10-60 mg/kg body weight, it induced up to 100-fold increase in ornithine decarboxylase activity with a maximum 16 h after its administration. These results suggest that MX is genotoxic and induces cell proliferation in the glandular stomach of rats.

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Inflammatory cell numbers in the stomach of Japanese subjects with endoscopically normal mucosa without H. pylori infection

Digestive Diseases ◽

10.1159/000515345 ◽

2021 ◽

Author(s):

Naoki Sumi ◽

Ken Haruma ◽

Tomoari Kamada ◽

Mitsuhiko Suehiro ◽

Noriaki Manabe ◽

...

Keyword(s):

Inflammatory Cells ◽

Normal Mucosa ◽

Mucosal Inflammation ◽

Upper Gastrointestinal Endoscopy ◽

Fundic Gland ◽

Eosinophilic Gastritis ◽

Pyloric Mucosa ◽

Sydney System ◽

Updated Sydney System ◽

H Pylori

Introduction: Since inflammatory cells, such as lymphocytes and plasma cells, normally inhabit the stomach, the border between normal and mild inflammation is difficult to visually determine using the updated Sydney system scale of gastritis. Additionally, eosinophils in the gastric mucosa must be counted to diagnose eosinophilic gastritis. We aimed to determine the normal number of inflammatory cells in patients with endoscopically normal mucosa and without H. pylori infections. Methods: We assessed patients aged 20–79 years, who had undergone upper gastrointestinal endoscopy at Kawasaki Medical School Hospital between January 2010 and December 2014. Inflammatory cells were counted in 1,000 μm2 fields of pyloric and fundic gland mucosal biopsy specimens. We finally included 325 (male, n = 141; female, n = 184; average age = 49.3 years) patients without inflammation who had H. pylori-negative endoscopic results and negative histological findings interpreted based on the updated Sydney System and the Kyoto classification of gastritis. Results: The average numbers of nucleated cells were 83.3 ± 14.2/mm2 and 65.4 ± 12.6/mm2 in the pyloric and fundic gland mucosae, respectively. Inflammatory cells were significantly more abundant in the pyloric mucosa than the fundic gland mucosa (p < 0.05). Age and sex distribution did not significantly differ. Eosinophils were absent or scanty in the gastric mucosae of both glands in all patients. Conclusion: We determined the absolute values of inflammatory cells, including eosinophils, in normal mucosae of pyloric and fundic glands. These findings could be important in defining gastric mucosal inflammation, including eosinophilic gastritis diagnosis.

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Aspects of the biology of regeneration and repair in the human gastrointestinal tract

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.1998.0257 ◽

1998 ◽

Vol 353 (1370) ◽

pp. 925-933 ◽

Cited By ~ 45

Author(s):

Nicholas A. Wright

Keyword(s):

Stem Cells ◽

Gastric Gland ◽

Cell Lineage ◽

Mucosal Ulceration ◽

Cell Lineages ◽

Trefoil Peptides ◽

Pyloric Mucosa ◽

A Cell ◽

Epidermal Growth ◽

Altered Gene

The main pathways of epithelial differentiation in the intestine, Paneth, mucous, endocrine and columnar cell lineages are well recognized. However, in abnormal circumstances, for example in mucosal ulceration, a cell lineage with features distinct from these emerges, which has often been dismissed in the past as ‘pyloric’ metaplasia, because of its morphological resemblance to the pyloric mucosa in the stomach. However, we can conclude that this cell lineage has a defined phenotype unique in gastrointestinal epithelia, has a histogenesis that resembles that of Brunner's glands, but acquires a proliferative organization similar to that of the gastric gland. It expresses several peptides of particular interest, including epidermal growth factor, the trefoil peptides TFF1, TFF2, TFF3, lysozyme and PSTI. The presence of this lineage also appears to cause altered gene expression in adjacent indigenous cell lineages. We propose that this cell lineage is induced in gastrointestinal stem cells as a result of chronic mucosal ulceration, and plays an important part in ulcer healing; it should therefore be added to the repertoire of gastrointestinal stem cells.

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