Journal
APOPTOSIS
Volume 23, Issue 7-8, Pages 377-387Publisher
SPRINGER
DOI: 10.1007/s10495-018-1464-9
Keywords
Acute pancreatitis; Gastrointestinal microecology; Intestinal barrier; Systemic inflammatory response syndrome; Enteral nutrition
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Funding
- National Nature Scientific Foundation of China [81100314, 81370565, 81770639]
- Nature Scientific Foundation of Heilongjiang Province [H201445]
- Wei-Han Yu scientific foundation of Harbin Medical University
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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.
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