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Infection and Immunity, September 2007, p. 4357-4363, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.01660-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Upregulation of CCL20 and Recruitment of CCR6⁺ Gastric Infiltrating Lymphocytes in Helicobacter pylori Gastritis

Yi-Ying Wu,^1, Hwei-Fang Tsai,^2,3, We-Cheng Lin,¹ Ping-I Hsu,⁴ Chia-Tung Shun,⁵ Ming-Shiang Wu,⁶ and Ping-Ning Hsu^1,6*

Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan,¹ Department of Internal Medicine, Taipei City Hospital, Ho-Ping Branch, Taipei, Taiwan,² Institute of Immunology, Chung-Shan Medical and Dental College, Taichung, Taiwan,³ Department of Internal Medicine, Veterans General Hospital-Kaohsiung, Kaohsiung, Taiwan,⁴ Department of Pathology, National Taiwan University Hospital, Taipei, Taiwan,⁵ Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan⁶

Received 17 October 2006/ Returned for modification 27 December 2006/ Accepted 4 June 2007

Helicobacter pylori infection is associated with an inflammatory response in the gastric mucosa, leading to chronic gastritis, peptic ulcers, and gastric cancer. There is increased T-cell infiltration at the site of infection with H. pylori. CCR6, a specific ß-chemokine receptor for CCL20 (MIP-3/LARC/exodus), has recently been reported to mediate lymphocyte homeostasis and immune responses in mucosal tissue, and it may play a role in chemokine-mediated lymphocyte trafficking during gastric inflammation. In this study, we investigated the role of CCR6 and its ligand, CCL20, in inducing an inflammatory response in the gastric mucosa during H. pylori infection. Gastric infiltrating T lymphocytes were isolated from endoscopic biopsy specimens of H. pylori gastritis patients and analyzed for the expression of the CCR6 chemokine receptor. Our results demonstrated that there was significantly increased CCR6 expression in CD3⁺ T cells infiltrating the gastric mucosa, and the CCR6 ligand, the CCL20 chemokine, was selectively expressed in inflamed gastric tissues. The production of CCL20 was upregulated in response to H. pylori in gastric epithelial cells when there was stimulation by the proinflammatory cytokines interleukin-1ß and tumor necrosis factor alpha. Furthermore, recombinant CCL20 induced lymphocyte chemotaxis migration in fresh gastric T cells ex vivo, indicating that the gastric T cells could migrate toward inflammatory sites via CCR6/CCL20 interaction. Our results suggest that the interaction between CCL20 and CCR6 may play a role in chemokine-mediated lymphocyte trafficking during gastric inflammation in Helicobacter infection.

Published ahead of print on 11 June 2007.

Editor: R. P. Morrison

Y.-Y.W. and H.-F.T. contributed equally to this work.

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