Gastrointestinal microecology: a crucial and potential target in acute pancreatitis
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 MO...
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Published in | Apoptosis (London) Vol. 23; no. 7-8; pp. 377 - 387 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Springer US
01.08.2018
Springer Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | 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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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1360-8185 1573-675X |
DOI: | 10.1007/s10495-018-1464-9 |