The intestinal barrier as a “firewall” in acute pancreatitis: dysbiosis and the cascade of complications

Emergency Medicine (Ukraine) · Published 2026-05-10 · DOI 10.22141/2224-0586.22.3.2026.2015

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Abstract

Background. Acute pancreatitis (AP) is a heterogeneous systemic inflammatory syndrome in which early failure of the intestinal barrier and gut dysbiosis promote endotoxemia, translocation of microbial products, and increased systemic complications. Objective: to synthesize current evidence on the role of the gut barrier and microbiota in AP complications, outline key mechanistic links, and highlight how multi-omics biomar­kers may support early risk stratification. Materials and methods. Narrative synthesis with a structured search. PubMed/Medline, Scopus, and Google Scholar were searched. We included clinical and experimental stu­dies assessing microbiota/metabolites and relevant outcomes (organ failure, infected pancreatic necrosis, sepsis, acute respiratory distress syndrome, mortality). Results. Evidence indicates an early rise in intestinal permeability in AP, associated with disease severity and enabling dysbiosis and microbial translocation, particularly in necrotizing phenotypes. The most reproducible taxonomic shifts include increases in Enterococcus/Enterobacteriaceae/Escherichia-Shigella and decreases in Bifidobacterium/Blautia, which in se­veral cohorts correlate with intensive care need, infectious complications, and pulmonary involvement. Integrative approaches (metagenomics + metabolomics) reveal signatures linked to the risk of organ failure/acute respiratory di­stress syndrome, while microbiota-derived metabolites (short-chain fatty acids, bile acids, aromatic toxins) provide a functional layer that can improve prognostic models when combined with clinical variables. ­Conclusions. The gut barrier and microbiota are pivotal drivers of the AP complication cascade. Clinical translation of microbiome-based biomarkers requires standardized preanalytics/analytics, very early sampling, rigorous confounder control, and external validation on independent cohorts.

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Publication details

Year
2026

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