TY - JOUR
T1 - Enhanced expression of CXCL13 in human helicobacter pylori-associated gastritis
AU - Nakashima, Yujiro
AU - Isomoto, Hajime
AU - Matsushima, Kayoko
AU - Yoshida, Akira
AU - Nakayama, Toshiyuki
AU - Nakayama, Masaaki
AU - Hisatsune, Junzo
AU - Ichikawa, Tatsuki
AU - Takeshima, Fuminao
AU - Hayashi, Tomayoshi
AU - Nakao, Kazuhiko
AU - Hirayama, Toshiya
AU - Kohno, Shigeru
PY - 2011/10/1
Y1 - 2011/10/1
N2 - Background and Aims: Chemokine CXC ligand 13 (CXCL13) and CXC receptor type 5 (CXCR5) are constitutively expressed in tertiary lymphoid follicles where the CXCL13/CXCR5 system regulates B lymphocytes homing. In this study, we sought to examine CXCL13 expression in the H. pylori-infected and -uninfected gastric mucosa and to elucidate the implication in the pathogenesis of HAG in humans. Methods: Using endoscopic biopsies taken from the gastric antrum of 29 subjects infected with Helicobacter pylori and 22 uninfected subjects, mucosal CXCL13 mRNA and protein levels were measured by real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Results: The CXCL13 expression levels were significantly more elevated in H. pylori-positive patients than uninfected ones. The CXCL13 expression levels correlated with the degree of chronic gastritis and bacterial colonization. Immunohistochemistry and in vitro infection assay showed that CXCL13 was not produced by the gastric epithelium, but the α-smooth muscle antigen expressing mesenchymal cells were the possible source of CXCL13 within H. pylori-infected gastric mucosa. CXCR5 immunostaining was seen in the CD20-positive lymphoid aggregates. Conclusions: The enhanced induction of CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis.
AB - Background and Aims: Chemokine CXC ligand 13 (CXCL13) and CXC receptor type 5 (CXCR5) are constitutively expressed in tertiary lymphoid follicles where the CXCL13/CXCR5 system regulates B lymphocytes homing. In this study, we sought to examine CXCL13 expression in the H. pylori-infected and -uninfected gastric mucosa and to elucidate the implication in the pathogenesis of HAG in humans. Methods: Using endoscopic biopsies taken from the gastric antrum of 29 subjects infected with Helicobacter pylori and 22 uninfected subjects, mucosal CXCL13 mRNA and protein levels were measured by real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Results: The CXCL13 expression levels were significantly more elevated in H. pylori-positive patients than uninfected ones. The CXCL13 expression levels correlated with the degree of chronic gastritis and bacterial colonization. Immunohistochemistry and in vitro infection assay showed that CXCL13 was not produced by the gastric epithelium, but the α-smooth muscle antigen expressing mesenchymal cells were the possible source of CXCL13 within H. pylori-infected gastric mucosa. CXCR5 immunostaining was seen in the CD20-positive lymphoid aggregates. Conclusions: The enhanced induction of CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis.
KW - CXC receptor type 5
KW - Chemokine CXC ligand 13
KW - Chronic inflammation
KW - Helicobacter pylori
KW - α-Smooth muscle antigen
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U2 - 10.1007/s10620-011-1717-8
DO - 10.1007/s10620-011-1717-8
M3 - Article
C2 - 21647655
AN - SCOPUS:80054748386
VL - 56
SP - 2887
EP - 2894
JO - American Journal of Digestive Diseases
JF - American Journal of Digestive Diseases
SN - 0002-9211
IS - 10
ER -