Abstract
Although T cell involvement in Helicobactor pylori-induced gastritis is known, mechanism about T cell recruitment is not understood. In this study we examined how mucosal addressin cell adhesion molecule-1 (MAdCAM-1) is involved in lymphocyte recruitment in murine chronic gastritis induced by H. pylori. C57 BL/6 mice were infected with Sydney strain (SS1). Six months after infection, the stomach was removed. The expression of adhesion molecules, MAdCAM-1, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and the cell surface antigens CD4, CD8, CD45R/B220 or β7-integrin were determined by immunohistochemistry. A significant increase in CD4 lymphocytes was observed in the body portion of stomach in SS1-infected mice and most of these CD4 cells express β7-integrin, a known counter ligand for MAdCAM-1 molecule. Strong MAdCAM-1 expression was observed adjacent to these cells in the lamina propria as well as in the submucosa of SS1-infected stomach. Quantitative analysis showed that the area of MAdCAM-1 expression well correlated with the infiltration of β7-integrin positive lymphocytes. On the other hand, expression of ICAM-1 or VCAM-1 in the lamina propria was few even in the SS1-infected stomach. Increased expression of MAdCAM-1 was well correlated to the location of lymphocytes, which express CD4 and β7-integrin. These results suggest the possibility that MAdCAM-1 may be largely involved in the lymphocyte recruitment in the gastritis mucosa with H. pylori.
| Original language | English |
|---|---|
| Pages (from-to) | 183-189 |
| Number of pages | 7 |
| Journal | Clinical and Experimental Immunology |
| Volume | 130 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2002 |
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Keywords
- β7-integrin
- Adhesion molecules
- Helicobactor pylori gastritis
- Lymphocyte migration mucosal addressin cell adhesion molecule-1 (MAdCAM-1)
ASJC Scopus subject areas
- Immunology
Cite this
Increased expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and lymphocyte recruitment in murine gastritis induced by Helicobacter pylori. / Hatanaka, K.; Hokari, R.; Matsuzaki, K.; Kato, S.; Kawaguchi, A.; Nagao, S.; Suzuki, Hidekazu; Miyazaki, K.; Sekizuka, E.; Nagata, H.; Ishii, H.; Miura, S.
In: Clinical and Experimental Immunology, Vol. 130, No. 2, 2002, p. 183-189.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Increased expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and lymphocyte recruitment in murine gastritis induced by Helicobacter pylori
AU - Hatanaka, K.
AU - Hokari, R.
AU - Matsuzaki, K.
AU - Kato, S.
AU - Kawaguchi, A.
AU - Nagao, S.
AU - Suzuki, Hidekazu
AU - Miyazaki, K.
AU - Sekizuka, E.
AU - Nagata, H.
AU - Ishii, H.
AU - Miura, S.
PY - 2002
Y1 - 2002
N2 - Although T cell involvement in Helicobactor pylori-induced gastritis is known, mechanism about T cell recruitment is not understood. In this study we examined how mucosal addressin cell adhesion molecule-1 (MAdCAM-1) is involved in lymphocyte recruitment in murine chronic gastritis induced by H. pylori. C57 BL/6 mice were infected with Sydney strain (SS1). Six months after infection, the stomach was removed. The expression of adhesion molecules, MAdCAM-1, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and the cell surface antigens CD4, CD8, CD45R/B220 or β7-integrin were determined by immunohistochemistry. A significant increase in CD4 lymphocytes was observed in the body portion of stomach in SS1-infected mice and most of these CD4 cells express β7-integrin, a known counter ligand for MAdCAM-1 molecule. Strong MAdCAM-1 expression was observed adjacent to these cells in the lamina propria as well as in the submucosa of SS1-infected stomach. Quantitative analysis showed that the area of MAdCAM-1 expression well correlated with the infiltration of β7-integrin positive lymphocytes. On the other hand, expression of ICAM-1 or VCAM-1 in the lamina propria was few even in the SS1-infected stomach. Increased expression of MAdCAM-1 was well correlated to the location of lymphocytes, which express CD4 and β7-integrin. These results suggest the possibility that MAdCAM-1 may be largely involved in the lymphocyte recruitment in the gastritis mucosa with H. pylori.
AB - Although T cell involvement in Helicobactor pylori-induced gastritis is known, mechanism about T cell recruitment is not understood. In this study we examined how mucosal addressin cell adhesion molecule-1 (MAdCAM-1) is involved in lymphocyte recruitment in murine chronic gastritis induced by H. pylori. C57 BL/6 mice were infected with Sydney strain (SS1). Six months after infection, the stomach was removed. The expression of adhesion molecules, MAdCAM-1, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), and the cell surface antigens CD4, CD8, CD45R/B220 or β7-integrin were determined by immunohistochemistry. A significant increase in CD4 lymphocytes was observed in the body portion of stomach in SS1-infected mice and most of these CD4 cells express β7-integrin, a known counter ligand for MAdCAM-1 molecule. Strong MAdCAM-1 expression was observed adjacent to these cells in the lamina propria as well as in the submucosa of SS1-infected stomach. Quantitative analysis showed that the area of MAdCAM-1 expression well correlated with the infiltration of β7-integrin positive lymphocytes. On the other hand, expression of ICAM-1 or VCAM-1 in the lamina propria was few even in the SS1-infected stomach. Increased expression of MAdCAM-1 was well correlated to the location of lymphocytes, which express CD4 and β7-integrin. These results suggest the possibility that MAdCAM-1 may be largely involved in the lymphocyte recruitment in the gastritis mucosa with H. pylori.
KW - β7-integrin
KW - Adhesion molecules
KW - Helicobactor pylori gastritis
KW - Lymphocyte migration mucosal addressin cell adhesion molecule-1 (MAdCAM-1)
UR - http://www.scopus.com/inward/record.url?scp=18644383871&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=18644383871&partnerID=8YFLogxK
U2 - 10.1046/j.1365-2249.2002.01984.x
DO - 10.1046/j.1365-2249.2002.01984.x
M3 - Article
C2 - 12390304
AN - SCOPUS:18644383871
VL - 130
SP - 183
EP - 189
JO - Clinical and Experimental Immunology
JF - Clinical and Experimental Immunology
SN - 0009-9104
IS - 2
ER -