Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, Heilongjiang, China.
Kidney Disease Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Apoptosis. 2018 Aug;23(7-8):377-387. doi: 10.1007/s10495-018-1464-9.
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.
在急性胰腺炎（AP）的早期阶段，由局部胰腺炎症引起的大量细胞因子进入血液，通过“触发效应”进一步引起全身炎症反应综合征（SIRS），最终导致多器官功能障碍综合征（MODS）。在 SIRS 和 MODS 期间，肠道屏障功能严重受损，同时发生肠道来源的感染，通过炎症过度产生形成“二次打击高峰”。胃肠道微生态，即生物屏障，在 AP 炎症应激的干扰下可能会转变为致病状态，这种状态被称为菌群失调。越来越多的证据表明，胃肠道微生态失调在 AP 肠道来源感染引起的“二次打击”中起着关键作用。因此，维持胃肠道微生态平衡可能为调节 AP 全身感染提供一种有效的方法。本文综述了胃肠道微生态在 AP 中的研究进展，为深入了解 AP 的发病机制和寻找新的治疗靶点提供参考。
