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Gastrointestinal microecology: a crucial and potential target in acute pancreatitis
Meng-Er Cen1,2,3, Feng Wang4, Ying Su4
1Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, Heilongjiang, China.
Abstract:
In the early stage of acute pancreatitis (AP), abundant cytokines induced by local pancreatic inflammation enter the bloodstream, further cause systemic inflammatory response syndrome (SIRS) by "trigger effect", which eventually leads to multiple organ dysfunction syndrome (MODS). During SIRS and MODS, the intestinal barrier function was seriously damaged accompanied by the occurrence of gut-derived infection which forms a "second hit summit" by inflammatory overabundance. Gastrointestinal microecology, namely the biologic barrier, could be transformed into a pathogenic state, which is called microflora dysbiosis when interfered by the inflammatory stress during AP. More and more evidences indicate that gastrointestinal microflora dysbiosis plays a key role in "the second hit" induced by AP gut-derived infection. Therefore, the maintenance of gastrointestinal microecology balance is likely to provide an effective method in modulating systemic infection of AP. This article reviewed the progress of gastrointestinal microecology in AP to provide a reference for deeply understanding the pathogenic mechanisms of AP and identifying new therapeutic targets.
Insights
Acute pancreatitis (AP) triggers systemic inflammation and organ dysfunction. Maintaining gut microecology balance is key to preventing secondary infections in AP.
Area of Science:
- Gastroenterology
- Microbiology
- Immunology
Background:
- Acute pancreatitis (AP) causes local inflammation, releasing cytokines that trigger systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS).
- During SIRS/MODS, intestinal barrier damage and gut-derived infections create a "second hit," exacerbating inflammation.
- Inflammatory stress in AP disrupts gastrointestinal microecology, leading to microflora dysbiosis, a critical factor in gut-derived infections.
Purpose of the Study:
- To review the role of gastrointestinal microecology in the pathogenesis of acute pancreatitis.
- To highlight the significance of microflora dysbiosis in AP-associated gut-derived infections.
- To identify potential therapeutic targets for modulating systemic infection in AP by maintaining gut health.
Main Methods:
- Literature review of studies on acute pancreatitis, systemic inflammatory response syndrome, multiple organ dysfunction syndrome, and gastrointestinal microecology.
- Analysis of the relationship between inflammatory cytokines, intestinal barrier function, and gut microbiota.
- Synthesis of evidence linking microflora dysbiosis to gut-derived infections and systemic complications in AP.
Main Results:
- Gastrointestinal microflora dysbiosis is a key factor in the "second hit" phenomenon during AP, driven by gut-derived infections.
- Imbalance in gut microecology contributes significantly to the severity of systemic inflammation and organ dysfunction in AP.
- Evidence suggests that preserving gastrointestinal microecology balance can mitigate AP-related systemic infections.
Conclusions:
- Gastrointestinal microecology plays a crucial role in the pathophysiology of acute pancreatitis.
- Microflora dysbiosis is implicated in the development of severe complications, including systemic infection, in AP.
- Targeting gastrointestinal microecology offers a promising therapeutic strategy for managing acute pancreatitis and its systemic consequences.
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