Open AccessUpregulation of CCL20 and Recruitment of CCR6 + Gastric Infiltrating Lymphocytes in Helicobacter pylori Gastritis
Author(s) -
YiYing Wu,
Hwei-Fang Tsai,
We-Cheng Lin,
PingI Hsu,
Chia–Tung Shun,
Ming–Shiang Wu,
Ping-Ning Hsu
Publication year - 2007
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.01660-06
Subject(s) - ccl20 , c c chemokine receptor type 6 , chemokine , gastric mucosa , biology , immunology , chemokine receptor , helicobacter pylori , gastritis , inflammation , stomach , biochemistry , genetics
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 withH. pylori . CCR6, a specific β-chemokine receptor for CCL20 (MIP-3α/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 duringH. pylori infection. Gastric infiltrating T lymphocytes were isolated from endoscopic biopsy specimens ofH. 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 toH. pylori in gastric epithelial cells when there was stimulation by the proinflammatory cytokines interleukin-1β 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 inHelicobacter infection.