AIM:The interaction of mucosal addressin cell adhesionmolecule 1 (MAdCAM-1) with integrin α4β7 mediateslymphocyte recruitment into mucosa-associated lymphoidtissue (MALT).Nodular gastritis is characterized by a uniquemilitary pattern on endoscopy representing increasednumbers of lymphoid follicles with germinal center,stronglyassociated with H pylori infection.The purpose of this studywas to address the implication of the MAdCAM-1/integrinβ7 pathway in NG.METHODS:We studied 17 patients with NG and H pyloriinfection and 19 H pylori-positive and 14 H pylori-negativecontrols.A biopsy sample was taken from the antrum andsnap-frozen for immunohistochemical analysis of MAdCAM-1 and integrin β7.In simultaneous viewing of serial sections,the percentage of MAdCAM-1-positive to von Willebrandfactor-positive vessels was calculated.We also performedimmunostaining with anti-CD20,CD4,CD8 and CD68antibodies to determine the lymphocyte subsets co-expressing integrin β7.RESULTS:Vascular endothelial MAdCAM-1 expression wasmore enhanced in gastric mucosa with than without H pyloriinfection.Of note,the percentages of MAdCAM-1-positivevessels were significantly higher in the lamina propria of NGpatients than in H pylori-positive controls.Strong expressionof MAdCAM-1 was identified adjacent to lymphoid folliclesand dense lymphoid aggregates.Integrin β7-expressingmononuclear cells,mainly composed of CD20 and CD4lymphocytes,were associated with vessels lined withMAdCAM-1-expressing endothelium.CONCLUSION: Our results suggest that the MAdCAM一1/integrin a4p7 homing system may participate in gastric inflammation in response to H py/o}i-infection and contributes to MALT formation, typically leading to the development of NG. 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 nurses 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 control. A biopsy simultaneous sampling of the serial sections, the percentage of MAdCAM-1-positive to von Willebrand factor-positive vessels was calculated. We also performed immunostaining with anti- CD20, CD4, CD8 and CD68 antibodies to determine the lymphocyte subsets co-expressing integrin β7.RESULTS: Vascular endothelia l MAdCAM-1 expression was more enhanced in gastric mucosa with than without H pylori infection. Of note, the percentages of MAdCAM-1-positivevessels were significantly higher in the lamina propria of NGpatients 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 a4p7 homing system may participate in gastric inflammation in response to H py / o} i-infection and contributes to MALT formation, typically leading to the development of NG.