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
收藏
页码:82 / 88
页数:6
相关论文
共 26 条
[1]  
Warren J.R., Unidentified curved bacilli on gastric epithelium in active chronic gastritis, Lancet, 1, pp. 1273-1275, (1983)
[2]  
Marshall B.J., Warren J.R., Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration, Lancet, 1, pp. 1311-1314, (1984)
[3]  
Lambert J.R., Dunn K.L., Eaves E.R., Korman M.G., Hansky J., Pinkard K.J., Pyloric CLO in the human stomach, Med J Aust, 143, (1985)
[4]  
Crabtree J.E., Wyatt J.I., Trejdosiewictz L.K., Peichl P., Nichols P.H., Ramsay N., Primrose J.N., Lindlet I.J.D., Interleukin-8 expression in Helicobacter pylori infected, normal and neoplastic gastroduodenal mucosa, J Clin Pathol, 47, pp. 61-66, (1994)
[5]  
Davies G.R., Banatvala N., Collins C.E., Sheaff T., Abdi Y., Clements L., Rampton D.S., Relationship between infective load of Helicobacter pylori and reactive oxygen metabolite production in antral mucosa, Scand J Gastroenterol, 29, pp. 419-424, (1994)
[6]  
Suzuki M., Miura S., Suematsu M., Eukumura D., Kuroe I., Suzuki H., Kai A., Kudoh Y., Ohashi M., Tsuchiya M., Helicobacter pylori-associated ammonia production enhances neutrophil-dependent gastric mucosal cell injury, Am J Physiol, 263, pp. G719-G725, (1992)
[7]  
Kaneko H., Nakada K., Mitsuma T., Uchida K., Furusawa A., Maeda Y., Helicobacter pylori infection induces a decrease in immunoreactive-somatostatin concentrations of human stomach, Dig Dis Sci, 37, pp. 409-416, (1992)
[8]  
Moss S.F., Legon S., Bishop A.E., Polak J.M., Calam J., Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease, Lancet, 340, pp. 930-932, (1992)
[9]  
Moss S.F., Calam J., Helicobacter pylori and peptic ulcers: The present position, Gut, 33, pp. 289-292, (1992)
[10]  
Beardshall K., Moss S.F., Gill J., Levi S., Ghosh P., Playford R.J., Calam J., Suppression of Helicobacter pylori reduces gastrin releasing peptide stimulated gastrin release in duodenal ulcer patients, Gut, 33, pp. 601-603, (1992)