IL-1β: a key modulator in asthmatic airway smooth muscle hyper-reactivity

被引:33
|
作者
Liao, Zhi [1 ,2 ,4 ]
Xiao, Hong-tao [2 ,3 ,4 ,5 ]
Zhang, Yuan [2 ,3 ,4 ,5 ]
Tong, Rong-Sheng [2 ,3 ,4 ,5 ]
Zhang, Li-Juan [2 ,3 ,4 ,5 ]
Bian, Yuan [2 ,3 ,4 ,5 ]
He, Xia [2 ,3 ,4 ,5 ]
机构
[1] Hosp Univ Elect Sci & Technol China, Dept Gynecol & Obstet, Chengdu, Peoples R China
[2] Sichuan Prov Peoples Hosp, Chengdu, Peoples R China
[3] Univ Elect Sci & Technol China, Sch Med, Chengdu 610054, Peoples R China
[4] Chinese Acad Sci, Sichuan Translat Med Hosp, Chengdu, Peoples R China
[5] Hosp Univ Elect Sci & Technol China, Dept Pharm, Chengdu, Peoples R China
关键词
asthma; IL-1; beta; hyperreactivity; muscarinic receptors; toll-like receptor; INTERLEUKIN-1 RECEPTOR ANTAGONIST; PARASYMPATHETIC GANGLIA; ALVEOLAR MACROPHAGES; LAVAGE FLUID; EXPRESSION; DISEASE; CYTOKINES; RELEASE; GENE; CELLS;
D O I
10.1586/17476348.2015.1063422
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Asthma is a chronic inflammatory disorder of the airway. It is characterized by airway hyper-reactivity, which can be attributed to the chronically inflamed airway. However, the molecular mechanism is still under investigation. In this article, we have shown that IL-1 beta is a key molecule that can orchestrate both Toll-like receptor and muscarinic receptor pathways, and that antagonizing the function of IL-1 beta has a promising future as a potential drug target for asthma treatment. IL-1 beta can activate NF-kappa B pathways via Toll-like receptors, and NF-kappa B will eventually transactivate the genes of cytokines, chemokines, proteins of the complement system, adhesion molecules and immune receptors involved in inflammation. IL-1 beta can activate eosinophils, which can release major basic protein (MBP) to antagonize the M-2 receptors leading to excessive acetylcholine release. Acetylcholine has an effect on M-3 receptors, which are related to airway smooth muscle contraction and mucus production. IL-1 beta is reported to activate COX-2 resulting in heterologous desensitization of adenylate cyclase and impairs relaxation of the ASM. IL-1 beta is involved in mediation of neutrophilic inflammation. Identification of the prominent role of IL-1 beta in asthma could lead to successful use of anti-IL1 beta agents.
引用
收藏
页码:429 / 436
页数:8
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