Abstract
Acute pancreatitis frequently causes intestinal barrier damage, which aggravates pancreatitis. Although Clostridium butyricum exerts anti-inflammatory and protective effects on the intestinal barrier during acute pancreatitis, the underlying mechanism is unclear. The G protein-coupled receptors 109 A (GPR109A) and adenosine monophosphate-activated protein kinase (AMPK)/ peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) signaling pathways can potentially influence the integrity of the intestinal barrier. Our study generated acute pancreatitis mouse models via intraperitoneal injection of cerulein and lipopolysaccharides. After intervention with Clostridium butyricum, the model mice showed reduced small intestinal and colonic intestinal barrier damage, dysbiosis amelioration, and increased GPR109A/AMPK/PGC-1α expression. In conclusion, Clostridium butyricum could improve pancreatic and intestinal inflammation and pancreatic injury, and relieve acute pancreatitis-induced intestinal barrier damage in the small intestine and colon, which may be associated with GPR109A/AMPK/PGC-1α.
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Funding
Our study was funded by the National Natural Science Foundation of China (No. 81870438), National Natural Science Foundation of Guangdong Province (No. 2022A1515010321), Guangzhou Technology Projects (N0.2023A03J0954), and Guangzhou Technology Projects (No. 202102020099).
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Guiqing Deng: Investigation, Formal analysis, Writing-Original Draft. Biyan Wen: Methodology, Project administration. Lin Jia: Conceptualization, Project administration. Jiaxin Liu: Software.
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Our study was approved by the Medical Ethics Committee of South China University of Technology. Permission certificate: SYXK (Guang dong)2022 − 0180; Validity: 2022/11/16-2027/11/15; Address: Laboratory Animal Center, B2 Building, South China University of Technology, Guangzhou University City, Guangzhou, China.
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Deng, G., Wen, B., Jia, L. et al. Clostridium butyricum upregulates GPR109A/AMPK/PGC-1α and ameliorates acute pancreatitis-associated intestinal barrier injury in mice. Arch Microbiol 206, 265 (2024). https://doi.org/10.1007/s00203-024-04001-8
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DOI: https://doi.org/10.1007/s00203-024-04001-8