Expression of mucosal addressin cell adhesion molecule 1 on vascular endothelium of gastric mucosa in patients with nodular gastritis

Hiroshi Ohara, Hajime Isomoto, Chun Yang Wen, Chieko Ejima, Masahiro Murata, Masanobu Miyazaki, Fuminao Takeshima, Yohei Mizuta, Ikuo Murata, Takehiko Koji, Hiroshi Nagura, Shigeru Kohno

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


Aim: The interaction of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) with integrin ?α4β7 mediates lymphocyte recruitment into mucosa-associated lymphoid tissue (MALT). Nodular gastritis is characterized by a unique military pattern on endoscopy representing increased numbers of lymphoid follicles with germinal center, strongly associated with H pylori infection. The purpose of this study was to address the implication of the MAdCAM-1/integrin β7 pathway in NG. Methods: We studied 17 patients with NG and H pylori infection and 19 H pylori-positive and 14 H pylori-negative controls. A biopsy sample was taken from the antrum and snap-frozen for immunohistochemical analysis of MAdCAM-1 and integrin β7. In simultaneous viewing of serial sections, the percentage of MAdCAM-1-positive to von Willebrand factor-positive vessels was calculated. We also performed immunostaining with anti-CD20, CD4, CDS and CD68 antibodies to determine the lymphocyte subsets coexpressing integrin β7. Results: Vascular endothelial MAdCAM-1 expression was more enhanced in gastric mucosa with than without H pylori infection. Of note, the percentages of MAdCAM-1-positive vessels were significantly higher in the lamina propria of NG patients than in H pylori-positive controls. Strong expression of MAdCAM-1 was identified adjacent to lymphoid follicles and dense lymphoid aggregates. Integrin β7-expressing mononuclear cells, mainly composed of CD20 and CD4 lymphocytes, were associated with vessels lined with MAdCAM-1-expressing endothelium. Conclusion: Our results suggest that the MAdCAM-1/ integrin α4β7 homing system may participate in gastric inflammation in response to H pylori-infection and contributes to MALT formation, typically leading to the development of NG.

Original languageEnglish
Pages (from-to)2701-2705
Number of pages5
JournalWorld Journal of Gastroenterology
Issue number12
Publication statusPublished - 12-2003

All Science Journal Classification (ASJC) codes

  • Gastroenterology


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