Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Am J Med Sci. 2021 Jan;361(1):43-54. doi: 10.1016/j.amjms.2020.07.030. Epub 2020 Jul 28.
Helicobacter pylori (H. pylori) infection causes inflammation and increases the risk of developing peptic ulcer disease (PUD); however, the exact molecular mechanisms of PUD development remain unclear. The aim of this study was to investigate the expression of CCL18, CCL28, and CXCL13 in H. pylori-positive subjects in comparison with H. pylori-negative subjects, and to determine its association with different clinical outcomes and virulence factors.
In total, 55 H. pylori-positive subjects with gastritis, 47 H. pylori-positive subjects with PUD, and 48 H. pylori-negative subjects were enrolled in this study. CCL18, CCL28, and CXCL13 expression were determined using real time polymerase chain reaction (PCR). The virulence factors of H. pylori such as cytotoxin-associated gene A (cagA), outer inflammatory protein A (oipA), blood group antigen-binding adhesin (babA), and vacuolating cytotoxin A (VacA) genes were evaluated using PCR.
CCL18, CCL28, and CXCL13 expression in H. pylori-positive subjects were significantly higher than H. pylori-negative subjects. CCL18 and CXCL13 expression in H. pylori-positive subjects with oipA and babA2were significantly higher than H. pylori-positive subjects with oipA¯ and babA2¯. CCL18 and CXCL13 expression were found to be significantly elevated in H. pylori-positive subjects with gastritis compared with H. pylori-positive subjects with PUD. CCL28 expression was significantly higher in H. pylori-positive subjects with PUD compared with H. pylori-positive subjects with gastritis.
The increased of CCL18 and CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis, while the increased of CCL28 may be involved in the pathogenesis of H. pylori-associated PUD.
幽门螺杆菌（H. pylori）感染会引起炎症，并增加患消化性溃疡病（PUD）的风险；然而，PUD 发展的确切分子机制仍不清楚。本研究旨在比较 H. pylori 阳性和 H. pylori 阴性受试者中 CCL18、CCL28 和 CXCL13 的表达，并确定其与不同临床结果和毒力因子的关系。
共纳入 55 例 H. pylori 阳性胃炎患者、47 例 H. pylori 阳性 PUD 患者和 48 例 H. pylori 阴性患者。采用实时聚合酶链反应（PCR）测定 CCL18、CCL28 和 CXCL13 的表达。采用 PCR 评估 H. pylori 的毒力因子，如细胞毒素相关基因 A（cagA）、外膜炎症蛋白 A（oipA）、血型抗原结合黏附素（babA）和空泡细胞毒素 A（VacA）基因。
H. pylori 阳性患者的 CCL18、CCL28 和 CXCL13 表达明显高于 H. pylori 阴性患者。H. pylori 阳性 oipA 和 babA2 患者的 CCL18 和 CXCL13 表达明显高于 H. pylori 阳性 oipA¯和 babA2¯患者。H. pylori 阳性胃炎患者的 CCL18 和 CXCL13 表达明显高于 H. pylori 阳性 PUD 患者。H. pylori 阳性 PUD 患者的 CCL28 表达明显高于 H. pylori 阳性胃炎患者。
CCL18 和 CXCL13 的增加可能参与了 H. pylori 相关胃炎的发病机制，而 CCL28 的增加可能参与了 H. pylori 相关 PUD 的发病机制。
