| Literature DB >> 29926313 |
Meng-Er Cen1,2,3, Feng Wang4, Ying Su4, Wang-Jun Zhang1, Bei Sun1, Gang Wang5.
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.Entities:
Keywords: Acute pancreatitis; Enteral nutrition; Gastrointestinal microecology; Intestinal barrier; Systemic inflammatory response syndrome
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Year: 2018 PMID: 29926313 DOI: 10.1007/s10495-018-1464-9
Source DB: PubMed Journal: Apoptosis ISSN: 1360-8185 Impact factor: 4.677