Ultrastructural evaluation of apoptosis induced by Helicobacter pylori infection in human gastric mucosa: Novel remarks on lamina propria mucosae

被引：5

作者：

Hasegawa C. ^{[1
]}

Ihara T. ^{[1
]}

Sugamata M. ^{[2
]}

机构：

[1] Department of Pathology, Tochigi Inst. of Clinical Pathology, Tochigi 329-0112, 2308-3, Minamiakatsuka

[2] Department of Pathology

来源：

Medical Electron Microscopy | 2000年 / 33卷 / 2期

关键词：

Apoptosis; Fibroblasts; Gastroduodenal ulcer; Helicobacter pylori; Smooth muscle cells; Ultrastructure;

D O I：

10.1007/s007950070006

中图分类号：

学科分类号：

摘要：

It has been considered that Helicobacter priori (H. priori) infection is a major cause of human gastritis and gastroduodenal ulcers (G-DU). Many investigations of the relationship between H. priori and apoptosis have been reported recently. However, these studies focused mostly on epithelium, using the TUNEL method. In the present study, we evaluated by electron microscopy the occurrence of apoptosis in the mesenchymal cells of lamina propria mucosae infected with H. pylori. Gastric biopsy specimens from 37 H. pylori-infected G-DU patients and 8 non-infected volunteers were examined with both light and electron microscopy and analyzed by the TUNEL method. The TUNEL method showed no significant difference between H. priori-infected and noninfected cases. In contrast, electron microscopy revealed significant numbers of apototic fibroblasts and smooth muscle cells in H. pylori-infected lamina propria mucosae, with a diminished number of collagen fibers in surrounding areas. These areas showed edematous changes histopathologically. These results indicated that H. pylori infection induces apoptosis of fibroblasts and smooth muscle cells in lamina propria, with decrease in the numbers of collagen fibers, suggesting that these alterations may be affected by exaggerate acid secretion, decrease mucus protecting factors, and result in ulcer formation.

引用

页码：82 / 88

页数：6

共 26 条

[11]

Davenport H.W., Warner H.A., Code C.F., Functional significance of gastric mucosal barrier to sodium, Gastroenterology, 42, pp. 142-152, (1964)

[12]

Moss S.F., Calam J., Agarwal B., Wang S., Holt P.R., Induction of gastric epithelial apoptosis by Helicobacter pylori, Gut, 38, pp. 498-501, (1996)

[13]

Jones N.L., Shannon P.T., Cutz E., Yeger H., Sherman M., Increase in proliferation and apoptosis of gastric epithelial cell early in the natural history of Helicobacter pylori infection, Am J Pathol, 151, pp. 1695-1703, (1997)

[14]

Kerr J.F.R., Wyllie A.H., Currie A.R., Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics, Br J Cancer, 26, pp. 236-257, (1972)

[15]

Tomei L.D., Cope F.O., Apoptosis: the molecular basis of cell death, (1994)

[16]

Ihara T., Yamamoto T., Sugamata M., Okamura H., Ueno Y., The process of ultrastructural changes from nuclei to apoptotic body, Virchows Arch, 433, pp. 433-437, (1998)

[17]

Yasuda M., Umemura S., Osamura R.Y., Kenjo T., Tsutsumi Y., Apoptosis cells in the human endometrium and placental villi: Pitfalls in applying the TUNEL method, Arch Histol Cytol, 58, pp. 185-190, (1995)

[18]

Lipkim M., Sherlock P., Bell B., Cell proliferation kinetics in the gastrointestinal tract in man. II. Cell renewal in stomac, ileum, colon and rectum, Gastroenterology, 45, pp. 721-729, (1963)

[19]

Gavrieli Y., Sherman Y., Ben-Sasson S.A., Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation, J Cell Biol, 119, pp. 493-501, (1992)

[20]

Hui P.K., Chan W.Y., Cheung P.S., Chan J.K.C., Ng C.S., Pathologic change of gastric mucosa colonized by Helicobacter pylori, Hum Pathol, 23, pp. 548-556, (1992)

← 1 2 3 →