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急性胰腺炎中的损伤相关分子模式和中性粒细胞胞外诱捕网。

Damage associated molecular patterns and neutrophil extracellular traps in acute pancreatitis.

机构信息

Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

School of the First Clinical Medical Sciences, Wenzhou Medical University, Wenzhou, China.

出版信息

Front Cell Infect Microbiol. 2022 Aug 12;12:927193. doi: 10.3389/fcimb.2022.927193. eCollection 2022.

DOI:10.3389/fcimb.2022.927193
PMID:36034701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9411527/
Abstract

Previous researches have emphasized a trypsin-centered theory of acute pancreatitis (AP) for more than a century. With additional studies into the pathogenesis of AP, new mechanisms have been explored. Among them, the role of immune response bears great importance. Pro-inflammatory substances, especially damage-associated molecular patterns (DAMPs), play an essential role in activating, signaling, and steering inflammation. Meanwhile, activated neutrophils attach great importance to the immune defense by forming neutrophil extracellular traps (NETs), which cause ductal obstruction, premature trypsinogen activation, and modulate inflammation. In this review, we discuss the latest advances in understanding the pathological role of DAMPs and NETs in AP and shed light on the flexible crosstalk between these vital inflammatory mediators. We, then highlight the potentially promising treatment for AP targeting DAMPs and NETs, with a focus on novel insights into the mechanism, diagnosis, and management of AP.

摘要

先前的研究已经强调了一个多世纪以来以胰蛋白酶为中心的急性胰腺炎 (AP) 理论。随着对 AP 发病机制的进一步研究,新的机制已经被探索出来。其中,免疫反应的作用非常重要。促炎物质,特别是损伤相关分子模式 (DAMPs),在激活、信号传递和引导炎症方面起着至关重要的作用。同时,激活的中性粒细胞通过形成中性粒细胞胞外陷阱 (NETs) 来重视免疫防御,NETs 会导致胆管阻塞、过早的胰蛋白酶原激活,并调节炎症。在这篇综述中,我们讨论了目前对 DAMPs 和 NETs 在 AP 中病理作用的理解的最新进展,并阐明了这些重要的炎症介质之间灵活的串扰。然后,我们重点介绍了针对 DAMPs 和 NETs 的潜在有希望的 AP 治疗方法,重点介绍了对 AP 的机制、诊断和管理的新见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0258/9411527/d5fd75bc5bab/fcimb-12-927193-g005.jpg
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