- 作者: Yi-Chun Yeh, Hsin-Yu Kuo, Wei-Lun Chang, Hsiao-Bai Yang, Cheng-Chan Lu, Hsiu-Chi Cheng, Ming-Shiang Wu and Bor-Shyang Sheu
- 作者服務機構: 1.Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan 2.Department of Internal Medicine, Tainan Hospital, Ministry of Health and Welfare, 125 Chuang Shan Road, Tainan, Taiwan 3.Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan 4.Department of Pathology, Ton Yen General Hospital, Hsin-Chu, Taiwan 5.Department of Pathology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan 6.Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan
- 中文摘要:
- 英文摘要:
Background
H. pylori CagL-Y58/E59 increase gastric cancer risk by stronger binding with integrin to faciliate type IV secretory system (T4SS). H. pylori can secrete high temperature requirement A (HtrA) to mediate E-Cadherin cleavage for gastric epithelial junction disruption, so H. pylori CagL can adhere to integrin located on basolateral side of epithelium. The study test whether H. pylori HtrA amino acid polymorphisms can increase gastric cancer risk synergistically with CagL-Y58/E59.
Methods
One-hundred and sixty-four H. pylori-positive patients, including 71 with non-ulcer dyspepsia (NUD), 63 with peptic ulcers (PU), and 30 with gastric cancers (GC), were enrolled to receive upper gastrointestinal endoscopy to obtain gastric biopsies for H. pylori culture and histology by the updated Sydney system. Each isolate was screened for htrA & cagL genotype by polymerase chain reaction and HtrA & CagL-Y58/E59 amino acid sequence polymorphisms by sequencing.
Results
The prevalence rates of htrA & cagL gene were both 100%. The HtrA amino acid sequence polymorphisms were not different between NUD and PU. The H. pylori isolates of GC had higher rates of HtrA residue 171 as leucine than those of NUD (73.3% vs. 50.7%, P = 0.036, OR[95%CI] = 2.7[1.1–6.8]). The risk of the H. pylori-infected subjects to get gastric cancer was increased up to 15.4-fold, if the infected isolates had presence of both HtrA-L171 and CagL-Y58/E59 (P < 0.001).
Conclusions
The H. pylori isolates of gastric cancer subjects had a higher rate of HtrA-L171. H. pylori isolates with presence of both HtrA-171 & CagL-Y58/E59 can synergistically increase the risk of gastric cancer. - 中文關鍵字:
- 英文關鍵字: Gastric cancer, H. pylori, HtrA, CagL, Type IV secretory system