Chun-Hua Zhou1, Yu-Ting Meng2, Jia-Jia Xu2, Xue Fang2, Jiu-Long Zhao2, Wei Zhou2, Jianhua Zhao3, Ji-Chen Han3, Ling Zhang4, Kai-Xuan Wang2, Liang-Hao Hu2, Zhuan Liao2, Wen-Bin Zou5, Zhao-Shen Li6, Duo-Wu Zou7. 1. Department of Gastroenterology, Changhai Hospital, The Second Military Medical University, No.168, Changhai Road, Yangpu District, Shanghai, 200433, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China; Department of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No.197, Rui Jin Er Road, Shanghai, 200025, China. 2. Department of Gastroenterology, Changhai Hospital, The Second Military Medical University, No.168, Changhai Road, Yangpu District, Shanghai, 200433, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China. 3. Shanghai Majorbio Bio-pharm Technology Co., Ltd., China. 4. Department of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No.197, Rui Jin Er Road, Shanghai, 200025, China. 5. Department of Gastroenterology, Changhai Hospital, The Second Military Medical University, No.168, Changhai Road, Yangpu District, Shanghai, 200433, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China. Electronic address: dr.wenbinzou@hotmail.com. 6. Department of Gastroenterology, Changhai Hospital, The Second Military Medical University, No.168, Changhai Road, Yangpu District, Shanghai, 200433, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China. Electronic address: zhaoshen-li@hotmail.com. 7. Department of Gastroenterology, Changhai Hospital, The Second Military Medical University, No.168, Changhai Road, Yangpu District, Shanghai, 200433, China; Shanghai Institute of Pancreatic Diseases, Shanghai, China; Department of Gastroenterology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No.197, Rui Jin Er Road, Shanghai, 200025, China. Electronic address: zdw_pi@163.com.
Abstract
BACKGROUND/ OBJECTIVES: Gut microbiota alterations in chronic pancreatitis (CP) are seldomly described systematically. It is unknown whether pancreatic exocrine insufficiency (PEI) and different etiologies in patients with CP are associated with gut microbiota dysbiosis. METHODS: The fecal microbiota of 69 healthy controls (HCs) and 71 patients with CP were compared to investigate gut microbiome alterations in CP and the relationship among gut microbiome dysbiosis, PEI and different etiologies. Fecal microbiomes were analyzed through 16S ribosomal RNA gene profiling, based on next-generation sequencing. Pancreatic exocrine function was evaluated by determining fecal elastase 1 activity. RESULTS: Patients with CP showed gut microbiota dysbiosis with decreased diversity and richness, and taxa-composition changes. On the phylum level, the gut microbiome of the CP group showed lower Firmicutes and Actinobacteria abundances than the HC group and higher Proteobacteria abundances. The abundances of Escherichia-Shigella and other genera were high in gut microbiomes in the CP group, whereas that of Faecalibacterium was low. Kyoto Encyclopedia of Genes and Genomes pathways (lipopolysaccharide biosynthesis and bacterial invasion of epithelial cells) were predicted to be enriched in the CP group. Among the top 5 phyla and 8 genera (in terms of abundance), only Fusobacteria and Eubacterium rectale group showed significant differences between CP patients, with or without PEI. Correlation analysis showed that Bifidobacterium and Lachnoclostridium correlated positively with fecal elastase 1 (r = 0.2616 and 0.2486, respectively, P < 0.05). CONCLUSIONS: The current findings indicate that patients with CP have gut microbiota dysbiosis that is partly affected by pancreatic exocrine function.
BACKGROUND/ OBJECTIVES: Gut microbiota alterations in chronic pancreatitis (CP) are seldomly described systematically. It is unknown whether pancreatic exocrine insufficiency (PEI) and different etiologies in patients with CP are associated with gut microbiota dysbiosis. METHODS: The fecal microbiota of 69 healthy controls (HCs) and 71 patients with CP were compared to investigate gut microbiome alterations in CP and the relationship among gut microbiomedysbiosis, PEI and different etiologies. Fecal microbiomes were analyzed through 16S ribosomal RNA gene profiling, based on next-generation sequencing. Pancreatic exocrine function was evaluated by determining fecal elastase 1 activity. RESULTS:Patients with CP showed gut microbiota dysbiosis with decreased diversity and richness, and taxa-composition changes. On the phylum level, the gut microbiome of the CP group showed lower Firmicutes and Actinobacteria abundances than the HC group and higher Proteobacteria abundances. The abundances of Escherichia-Shigella and other genera were high in gut microbiomes in the CP group, whereas that of Faecalibacterium was low. Kyoto Encyclopedia of Genes and Genomes pathways (lipopolysaccharide biosynthesis and bacterial invasion of epithelial cells) were predicted to be enriched in the CP group. Among the top 5 phyla and 8 genera (in terms of abundance), only Fusobacteria and Eubacterium rectale group showed significant differences between CP patients, with or without PEI. Correlation analysis showed that Bifidobacterium and Lachnoclostridium correlated positively with fecal elastase 1 (r = 0.2616 and 0.2486, respectively, P < 0.05). CONCLUSIONS: The current findings indicate that patients with CP have gut microbiota dysbiosis that is partly affected by pancreatic exocrine function.
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