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NLRP3 炎症小体调控机制在结肠炎中的矛盾效应。

Contradictory Effects of NLRP3 Inflammasome Regulatory Mechanisms in Colitis.

机构信息

Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Minami 1-jo Nishi 16-chome, Chuo-ku, Sapporo, Hokkaido 060-8543, Japan.

出版信息

Int J Mol Sci. 2020 Oct 30;21(21):8145. doi: 10.3390/ijms21218145.

Abstract

The inflammasome is an intracellular molecular complex, which is mainly involved in innate immunity. Inflammasomes are formed in response to danger signals, associated with infection and injury, and mainly regulate the secretion of interleukin-1β and interleukin-18. Inflammasome dysregulation is known to be associated with various diseases and conditions, and its regulatory mechanisms have become of great interest in recent years. In the colon, inflammasomes have been reported to be associated with autophagy and the microbiota, and their dysregulation contributes to colitis and. However, the detailed role of inflammasomes in inflammatory bowel disease is still under debate because the mechanisms that regulate the inflammasome are complex and the inflammasome components and cytokines show seemingly contradictory multiple effects. Herein, we comprehensively review the literature on inflammasome functioning in the colon and describe the complex interactions of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome components with inflammatory cytokines, autophagy, and the microbiota in experimental colitis models and patients with inflammatory bowel disease.

摘要

炎症小体是一种细胞内的分子复合物,主要参与固有免疫。炎症小体是对感染和损伤相关的危险信号做出反应而形成的,主要调节白细胞介素-1β和白细胞介素-18 的分泌。炎症小体的失调与各种疾病和病症有关,其调节机制近年来引起了极大的关注。在结肠中,炎症小体与自噬和微生物群有关,其失调导致结肠炎和。然而,炎症小体在炎症性肠病中的详细作用仍存在争议,因为调节炎症小体的机制很复杂,炎症小体的成分和细胞因子表现出看似矛盾的多种作用。在此,我们全面回顾了炎症小体在结肠中的作用的文献,并描述了 NOD 样受体家族富含吡喃结构域蛋白 3(NLRP3)炎症小体成分与炎症性细胞因子、自噬和微生物群在实验性结肠炎模型和炎症性肠病患者中的复杂相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53dd/7662299/af00683962be/ijms-21-08145-g001.jpg

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