Department of Medicine, University of Washington School of Medicine, Seattle, Washington.
Department of Medicine, Columbia University Irving Medical Center, New York, New York.
Cancer Epidemiol Biomarkers Prev. 2019 Oct;28(10):1687-1693. doi: 10.1158/1055-9965.EPI-19-0008. Epub 2019 Aug 29.
The incidence of esophageal adenocarcinoma has risen dramatically over the past half century, and the underlying reasons are incompletely understood. Broad shifts to the upper gastrointestinal microbiome may be partly responsible. The goal of this study was to describe alterations in the esophageal microbiome that occur with progression from Barrett's esophagus to esophageal adenocarcinoma.
A case-control study was performed of patients with and without Barrett's esophagus who were scheduled to undergo upper endoscopy. Demographic, clinical, and dietary intake data were collected, and esophageal brushings were collected during the endoscopy. 16S rRNA gene sequencing was performed to characterize the microbiome.
A total of 45 patients were enrolled and included in the analyses [16 controls; 14 Barrett's esophagus without dysplasia (NDBE); 6 low-grade dysplasia (LGD); 5 high-grade dysplasia (HGD); and 4 esophageal adenocarcinoma]. There was no difference in alpha diversity between non-Barrett's esophagus and Barrett's esophagus, but there was evidence of decreased diversity in patients with esophageal adenocarcinoma as assessed by Simpson index. There was an apparent shift in composition at the transition from LGD to HGD, and patients with HGD and esophageal adenocarcinoma had decreased Firmicutes and increased Proteobacteria. In addition, patients with HGD or esophageal adenocarcinoma had increased and and reduced . In the study population, patients taking proton pump inhibitors had increased and decreased Gram-negative bacteria overall.
Shifts in the Barrett's esophagus-associated microbiome were observed in patients with HGD and esophageal adenocarcinoma, with increases in certain potentially pathogenic bacteria.
The microbiome may play a role in esophageal carcinogenesis.
在过去的半个世纪中,食管腺癌的发病率急剧上升,其根本原因尚不完全清楚。上消化道微生物组的广泛变化可能是部分原因。本研究的目的是描述从 Barrett 食管发展为食管腺癌时食管微生物组的变化。
对计划进行上消化道内镜检查的 Barrett 食管患者和非 Barrett 食管患者进行病例对照研究。收集人口统计学、临床和饮食摄入数据,并在内镜检查期间采集食管刷检标本。进行 16S rRNA 基因测序以描述微生物组。
共纳入 45 例患者进行分析[16 例对照;14 例无异型增生的 Barrett 食管(NDBE);6 例低级别异型增生(LGD);5 例高级别异型增生(HGD);4 例食管腺癌]。非 Barrett 食管与 Barrett 食管之间的 alpha 多样性无差异,但 HGD 和食管腺癌患者的 Simpson 指数表明多样性降低。从 LGD 到 HGD 的过渡中存在明显的组成变化,HGD 和食管腺癌患者的Firmicutes减少,Proteobacteria增加。此外,HGD 或食管腺癌患者的增加,减少。在研究人群中,服用质子泵抑制剂的患者总体上增加了和减少了革兰氏阴性菌。
在 HGD 和食管腺癌患者中观察到 Barrett 食管相关微生物组的变化,某些潜在致病性细菌的增加。
微生物组可能在食管癌变中起作用。