ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Bifidobacterium Pseudolongum-Derived Acetate Attenuates Acute Pancreatitis Through GPR43-Mediated Suppression of M1 Macrophage Polarization.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Gut microbiota-host co-metabolism in hypertriglyceridemia-associated acute pancreatitis: from causality to precision intervention.Frontiers in immunology · 2026Review
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Authors and funding
17 authors.
Funding
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.
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Registered trials
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