20 July 2026 : Review article
The Roles of Gut Microbiota in the Pathogenesis of Acute Pancreatitis
Jun-Hua Ming BCDEF 1, Chang Chen EF 1, Jie Li D 1,2, Jie Gao E 1,2, Qing Zhang DG 1,2,3*DOI: 10.12659/MSM.952647
Med Sci Monit 2026; 32:e952647
Figure 2 The gut microbial-metabolic-immune axis in acute pancreatitis. This schematic summarizes how gut microbiota dysbiosis influences the severity of acute pancreatitis through immune and metabolic pathways. Intestinal dysbiosis leads to the release of pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide (LPS). These PAMPs activate Toll-like receptors (TLR2 and TLR4) on immune and epithelial cells, triggering the myeloid differentiation primary response 88 (MyD88)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway and promoting a proinflammatory response. Disrupted microbial metabolites can also activate nucleotide-binding oligomerization domain 1 (NOD1), further enhancing NF-κB activation and neutrophil infiltration, thereby exacerbating acute pancreatitis. In contrast, under physiological conditions, beneficial metabolites such as butyrate and microbial-derived proteins (eg, Amuc_1100) inhibit NF-κB signaling and attenuate inflammation. A reduction in regulatory T cells can destabilize the intestinal immune barrier, promoting bacterial translocation (BT) and worsening disease severity. This complex interplay highlights the central role of the gut microbiota in modulating both local intestinal and systemic inflammatory responses during acute pancreatitis.