Key Immunopathology Laboratory of Guangdong Province, Institute of Clinical Pathology & Department of Pathology, Shantou University Medical College, Shantou, Guangdong, China; Shaanxi Provincial People's Hospital, The Third Affiliated Hospital, Medical College of Xi'an Jiaotong University, Xi'an, China.
Int J Cancer. 2014 Jun 1;134(11):2626-32. doi: 10.1002/ijc.28588. Epub 2013 Nov 20.
Helicobacter pylori (H. pylori), a common pathogen residing in the gastrointestinal tract, has been well characterized in stomach cancer,while its correlation with esophageal cancer remains poorly understood. In this study, we aim to assess the relationship between esophageal intraepithelial H. pylori invasion and inflammation as well as atypical hyperplasia in esophageal squamous epithelial tissues. Esophageal squamous cell carcinoma (ESCC) tissue samples from 196 individuals from both southern and northern esophageal carcinoma high-risk areas in China were examined (125 from northern high-risk areas, 71 from southern high-risk area), while additional 30 samples were collected adjacent to the esophageal squamous cell carcinoma (A-ESCC). H. pylori infection was identified by Giemsa staining, immuno-histochemical staining, and H. pylori 16S rRNA-based PCR. A significant increase of H. pylori infection was found in tumor tissues (including ESCC and A-ESCC samples) compared to that of non-tumor tissues (p < 0.05). The positive rate of H. pylori 16S rRNA in ESCC, A-ESCC, and normal groups were 62.5, 74.1, and 26.7%, respectively. The PCR results showed that the positive incidence of the H. pylori virulence factor CagA gene in tumor (ESCC and A-ESCC) and normal groups was 54.9 and 20%, respectively (p < 0.05). To explore the possible causes of CagA+ H. pylori infection leading to carcinogenesis, we found that CagA+ H. pylori filtrate induced DNA strand breaks in esophageal epithelial NE3 cells, suggesting that H. pylori infection may be an original cause leading to atypical hyperplasia of esophageal squamous epithelial tissues and contributed to pathological carcinogenesis of ESCC.
幽门螺杆菌（H. pylori）是一种常见的胃肠道病原体，其与胃癌的关系已得到充分研究，而与食管癌的关系则知之甚少。本研究旨在评估食管上皮内 H. pylori 侵袭与炎症以及食管鳞状上皮组织不典型增生之间的关系。本研究共检测了来自中国南北食管癌高发区的 196 例食管鳞癌组织样本（北方高发区 125 例，南方高发区 71 例），另外还收集了 30 例食管鳞癌旁组织（A-ESCC）。通过吉姆萨染色、免疫组织化学染色和基于 H. pylori 16S rRNA 的 PCR 检测 H. pylori 感染。与非肿瘤组织相比，肿瘤组织（包括 ESCC 和 A-ESCC 样本）中 H. pylori 感染明显增加（p<0.05）。ESCC、A-ESCC 和正常组 H. pylori 16S rRNA 的阳性率分别为 62.5%、74.1%和 26.7%。PCR 结果显示，肿瘤（ESCC 和 A-ESCC）和正常组 H. pylori 毒力因子 CagA 基因的阳性率分别为 54.9%和 20%（p<0.05）。为了探讨 CagA+ H. pylori 感染导致癌变的可能原因，我们发现 CagA+ H. pylori 滤液可诱导食管上皮 NE3 细胞 DNA 链断裂，提示 H. pylori 感染可能是导致食管鳞状上皮组织不典型增生的原始原因，并促进 ESCC 的病理癌变。
