Akinari Sawada1, Yasuhiro Fujiwara2,3, Yasuaki Nagami1, Fumio Tanaka1,4, Hirokazu Yamagami1, Tetsuya Tanigawa1,5, Masatsugu Shiba1, Kazunari Tominaga1,5, Toshio Watanabe1,5, Min Gi6, Hideki Wanibuchi6, Tetsuo Arakawa1,5. 1. Department of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-7 Asahimachi, Abenoku, Osaka, 545-8585, Japan. 2. Department of Gastroenterology, Osaka City University Graduate School of Medicine, 1-4-7 Asahimachi, Abenoku, Osaka, 545-8585, Japan. yasu@med.osaka-cu.ac.jp. 3. SAMURAI GI Research Center, Osaka City University Graduate School of Medicine, 1-4-7 Asahimachi, Abenoku, Osaka, 545-8585, Japan. yasu@med.osaka-cu.ac.jp. 4. Department of Premier Preventive Medicine, Osaka City University Graduate School of Medicine, 1-4-7 Asahimachi, Abenoku, Osaka, 545-8585, Japan. 5. SAMURAI GI Research Center, Osaka City University Graduate School of Medicine, 1-4-7 Asahimachi, Abenoku, Osaka, 545-8585, Japan. 6. Department of Molecular Pathology, Osaka City University Graduate School of Medicine, 1-4-7 Asahimachi, Abenoku, Osaka, 545-8585, Japan.
Abstract
BACKGROUND: Recent studies suggest that chronic inflammation-associated cancer is relevant to microbiome. Esophageal adenocarcinoma arises from an inflammatory condition called Barrett's esophagus, which is caused by gastroesophageal reflux. We hypothesized that esophageal microbiome plays a role in carcinogenesis of esophageal adenocarcinoma. AIM: We investigated whether alteration of microbiome using antibiotics affects the development of esophageal adenocarcinoma in a rat model. METHODS: Seven-week-old male Wistar rats which had undergone esophagojejunostomy were divided into control (n = 21) and antibiotic groups (n = 22) at 21 weeks after surgery. Control animals were given drinking water, while the other group was given penicillin G and streptomycin in drinking water until rats were killed at 40 weeks after operation. Incidence rates of Barrett's esophagus and adenocarcinoma in each group were evaluated by histological analysis. DNA was extracted from a portion of the distal esophagus, and the microbiome was investigated using terminal restriction fragment length polymorphism (T-RFLP) analysis. RESULTS: All rats in both groups developed Barrett's esophagus. Incidence of esophageal adenocarcinoma was similar between both groups with a trend to reduced incidence in the antibiotics group (89 % in the control group, 71 % in the antibiotics group, P = 0.365). T-RFLP analysis showed that esophageal microbiome was different between two groups such as the proportion of Lactobacillales was lower in the antibiotics group and Clostridium cluster XIVa and XVIII was higher in the antibiotics group. CONCLUSIONS: Alteration of microbiome does not affect the incidence of esophageal adenocarcinoma. Microbiome may not contribute to the development of esophageal adenocarcinoma.
BACKGROUND: Recent studies suggest that chronic inflammation-associated cancer is relevant to microbiome. Esophageal adenocarcinoma arises from an inflammatory condition called Barrett's esophagus, which is caused by gastroesophageal reflux. We hypothesized that esophageal microbiome plays a role in carcinogenesis of esophageal adenocarcinoma. AIM: We investigated whether alteration of microbiome using antibiotics affects the development of esophageal adenocarcinoma in a rat model. METHODS: Seven-week-old male Wistar rats which had undergone esophagojejunostomy were divided into control (n = 21) and antibiotic groups (n = 22) at 21 weeks after surgery. Control animals were given drinking water, while the other group was given penicillin G and streptomycin in drinking water until rats were killed at 40 weeks after operation. Incidence rates of Barrett's esophagus and adenocarcinoma in each group were evaluated by histological analysis. DNA was extracted from a portion of the distal esophagus, and the microbiome was investigated using terminal restriction fragment length polymorphism (T-RFLP) analysis. RESULTS: All rats in both groups developed Barrett's esophagus. Incidence of esophageal adenocarcinoma was similar between both groups with a trend to reduced incidence in the antibiotics group (89 % in the control group, 71 % in the antibiotics group, P = 0.365). T-RFLP analysis showed that esophageal microbiome was different between two groups such as the proportion of Lactobacillales was lower in the antibiotics group and Clostridium cluster XIVa and XVIII was higher in the antibiotics group. CONCLUSIONS: Alteration of microbiome does not affect the incidence of esophageal adenocarcinoma. Microbiome may not contribute to the development of esophageal adenocarcinoma.
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