Interleukin-17 as a spatiotemporal bridge from acute to chronic inflammation: Novel insights from computational modeling.

IF 4.6 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
WIREs Mechanisms of Disease Pub Date : 2023-05-01 Epub Date: 2023-01-29 DOI:10.1002/wsbm.1599
Ashti M Shah, Ruben Zamora, Yoram Vodovotz
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引用次数: 0

Abstract

A systematic review of several acute inflammatory diseases ranging from sepsis and trauma/hemorrhagic shock to the relevant pathology of the decade, COVID-19, points to the cytokine interleukin (IL)-17A as being centrally involved in the propagation of inflammation. We summarize the role of IL-17A in acute inflammation, leveraging insights made possible by biological network analysis and novel computational methodologies aimed at defining the spatiotemporal spread of inflammation in both experimental animal models and humans. These studies implicate IL-17A in the cross-tissue spread of inflammation, a process that appears to be in part regulated through neural mechanisms. Although acute inflammatory diseases are currently considered distinct from chronic inflammatory pathologies, we suggest that chronic inflammation may represent repeated, cyclical episodes of acute inflammation driven by mechanisms involving IL-17A. Thus, insights from computational modeling of acute inflammatory diseases may improve diagnosis and treatment of chronic inflammation; in turn, therapeutics developed for chronic/autoimmune disease may be of benefit in acute inflammation. This article is categorized under: Immune System Diseases > Computational Models.

Abstract Image

白细胞介素-17 作为从急性炎症到慢性炎症的时空桥梁:来自计算模型的新见解。
对从败血症、创伤/失血性休克到本十年的相关病理 COVID-19 等几种急性炎症疾病的系统回顾表明,细胞因子白细胞介素 (IL)-17A 在炎症的传播中起着核心作用。我们总结了 IL-17A 在急性炎症中的作用,利用生物网络分析和新颖的计算方法,旨在确定炎症在实验动物模型和人类中的时空传播。这些研究表明,IL-17A 与炎症的跨组织扩散有关,而这一过程似乎部分是通过神经机制调节的。虽然急性炎症性疾病目前被认为有别于慢性炎症性病症,但我们认为慢性炎症可能是由涉及 IL-17A 的机制驱动的急性炎症的反复、周期性发作。因此,从急性炎症性疾病的计算模型中获得的见解可能会改善慢性炎症的诊断和治疗;反过来,为慢性/自身免疫性疾病开发的疗法可能会对急性炎症有益。本文归类于免疫系统疾病 > 计算模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
WIREs Mechanisms of Disease
WIREs Mechanisms of Disease MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
11.40
自引率
0.00%
发文量
45
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