Acute pancreatitis (AP), among the most common causes of acute abdomen, is characterized by persistent left upper abdominal pain and vomiting, without pain relief after vomiting.Its pathological features include abnormal activation of pancreatic enzymes and induction of pancreatic autodigestion by various etiologies.Emerging evidence indicates a strong association between the gut microbiota and AP progression, primarily mediated by intestinal barrier disruption, bacterial translocation, and immune dysregulation.Alterations in the gut microbiota, including overgrowth of pathogenic bacteria (eg, Enterobacteriaceae) and a reduction in beneficial commensals (eg, Lactobacillaceae and Bifidobacteriaceae), are consistently observed among patients with AP.The gut microenvironment, including factors such as bile acids, oxygen levels, and pH, shapes the microbial community and its interactions with the host.These changes can promote local and systemic inflammation, thereby exacerbating pancreatic necrosis and contributing to multiple organ dysfunction.Consequently, the bidirectional interaction between the gut microbiome and AP has received increasing attention.This review provides a comprehensive summary of the current understanding of how gut microbiota dysbiosis contributes to AP pathogenesis.We focus on mechanisms linking microbial and microenvironmental alterations to disease severity, including the roles of the gut-pancreas axis, short-chain fatty acids, and pattern recognition receptors.Finally, we discuss the potential of novel therapeutic strategies targeting these pathways for the management of AP.
Ming et al. (Thu,) studied this question.