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 1 Etiology-specific interactions between the gut microbiota and pancreatitis. This figure illustrates distinct interactions between the gut microbiota and the host across different etiologies of acute pancreatitis. (Left) In biliary pancreatitis, bacteria can migrate between the gallbladder and pancreas via the lymphatic system, promoting reciprocal inflammatory responses. Bile salts secreted into the intestine can disrupt gut microbiota composition by damaging bacterial DNA and cell membranes. Conversely, the gut microbiota regulates bile acid metabolism, thus influencing the risk and severity of biliary disease. (Center) In hypertriglyceridemia-induced acute pancreatitis, there is a reduced abundance of beneficial bacteria (eg, Bifidobacterium) and an overgrowth of Escherichia/Shigella and Enterococcus. Decreased microbial production of taurine, potentially by taxa such as Anaeroplasma, leads to increased colonic interleukin (IL)-17 levels and formation of neutrophil extracellular traps (NETs), which exacerbate pancreatic injury. (Right) In alcoholic pancreatitis, ethanol is metabolized by gut bacteria to acetaldehyde, which disrupts tight junctions and increases intestinal permeability. Together with increased small intestinal bacterial overgrowth, this facilitates bacterial translocation and aggravates pancreatic inflammation.