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Updated: Mar 30, 2026
Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
Published on: May 10, 2024
Bifidobacterium Pseudolongum-Derived Acetate Attenuates Acute Pancreatitis Through GPR43-Mediated Suppression of M1
Langyi Guan1, Xueyang Li1,2, Cong He1
1Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Abstract:
Acute pancreatitis (AP) is characterized by gut microbiota dysbiosis, which is marked by an expansion of pathogenic bacteria and a pronounced depletion of beneficial taxa, including Bifidobacterium. While Bifidobacterium pseudolongum (B. pseudolongum) possesses known probiotic properties, its potential role in protecting against AP has yet to be determined. This study shows that B. pseudolongum alleviates pancreatic damage, inflammation, and apoptosis in mice with caerulein-induced and pancreatic duct ligation-induced AP by enhancing gut barrier function and microbiota diversity. Metabolomics identifies acetate as its key metabolite, and the ackA gene is essential for acetate biosynthesis. Acetate supplementation protects against AP. Mechanistically, acetate acts via GPR43 to inhibit macrophage M1 polarization, and macrophage depletion abrogates this protection. Clinically, the fecal B. pseudolongum abundance is reduced in AP patients and is correlated with disease severity. These findings reveal a microbiota-metabolite-immune axis in AP and highlight the potential of B. pseudolongum and acetate supplementation as novel therapeutic strategies for AP.
Insights
Bifidobacterium pseudolongum protects against acute pancreatitis (AP) by improving gut health and reducing inflammation. Supplementing with this probiotic or its metabolite, acetate, shows therapeutic potential for AP patients.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Gut microbiota dysbiosis, characterized by pathogenic bacteria expansion and beneficial taxa depletion (e.g., Bifidobacterium), is a hallmark of acute pancreatitis (AP).
- Bifidobacterium pseudolongum (B. pseudolongum) is a probiotic with potential but unconfirmed protective effects against AP.
Purpose of the Study:
- To investigate the protective role of B. pseudolongum against acute pancreatitis.
- To elucidate the underlying mechanisms, including its key metabolites and immune interactions.
Main Methods:
- Induction of AP in mice using caerulein and pancreatic duct ligation.
- Administration of B. pseudolongum and acetate.
- Assessment of pancreatic damage, inflammation, apoptosis, gut barrier function, and microbiota diversity.
- Metabolomic analysis and gene essentiality assays (ackA).
- Macrophage polarization studies (GPR43) and depletion experiments.
- Clinical analysis of fecal B. pseudolongum abundance in AP patients.
Main Results:
- B. pseudolongum alleviated pancreatic damage, inflammation, and apoptosis in AP mouse models.
- It enhanced gut barrier function and microbiota diversity.
- Acetate was identified as a key metabolite produced by B. pseudolongum via the ackA gene; acetate supplementation also protected against AP.
- Acetate inhibited M1 macrophage polarization through GPR43, and this effect was crucial for protection.
- Reduced fecal B. pseudolongum abundance correlated with AP severity in patients.
Conclusions:
- B. pseudolongum demonstrates significant protective effects against acute pancreatitis.
- A microbiota-metabolite-immune axis involving B. pseudolongum, acetate, and macrophage polarization is critical in AP pathogenesis.
- B. pseudolongum and acetate supplementation represent promising therapeutic strategies for AP.
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