Hiroshima Journal of Medical Sciences Volume 33 Issue 2
published_at 1984-06

Histochemical and Ultrastructural Studies on Experimental Gastritis in Mice

実験胃炎の組織化学的電子顕徴鏡的研究
Tamaru Takaji
Okamoto Kazuma
Kambara Akihiko
Shimizu Satoru
Koh Hassei
Yamamoto Masahiro
Sano Kohichi
Daitoku Kunihiko
Kishimoto Shinya
Kajiyama Goro
fulltext
1.74 MB
HiroshimaJMedSci_33_137.pdf
Abstract
Experimental gastritis was produced in BALB/c (? / +) mice by the method of neonatal thymectomy. This atrophic gastritis was confined to the gastric fundobody mucosa and spared antrum. The morphological changes in the gastric mucosa of this type of gastritis have been described in detail during the growth process after thymectomy (1, 2, 3, 6, 10, and 15 months). The mucosal changes developed from the second months after thymectomy, which were characterized by destruction and degeneration of both the parietal and chief cells in the deep glands of gastric fundobody mucosa associated with cellular infiltration in the lamina propriae. From 3 to 6 months after the1 operation, however, the structure of the whole fundobody glands became composed of mostly immature cells and mucus-containing cells. These cells were similar in appearance to mucous neck cells of the normal stomach and stained positive with PAS-alcian blue at pH 2.5. At the ultrastructural level, however, the size, electron density and number of secretory granules of mucus-containing cells were different from those of cells of the normal stomach. During this period, both parietal and chief cells were markedly decreased in number and both cells were very immature. With growth (10 to 15 months after the operation), the mucosal thickness increased, although the cells composing the glands were essentially the same as those at the early to middle stages after the operation. Thus, this type of gastritis was characteristic of fundobody-confined atrophic gastritis associated with immature and undifferentiated cells as well as mucus-containing cells and hypertrophic mucosae. These peculiar changes in the gastric mucosae increased with growth after thymectomy.

The precise mechanism of induction of this type of gastritis still remains to be defined. However, first, the mucosal destruction and increased cellular proliferation are one of the possible causes, and secondly, unknown inhibitory mechanism for maturing immature cells can participate in the development of this type of gastritis. This is the other possible cause.
Keywords
Gastritis
Parietal cell
Chief cells
Prematured cell