title: IL-1β: a key modulator in asthmatic airway smooth muscle hyper-reactivity.
abstract: 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-1β is a key molecule that can orchestrate both Toll-like receptor and muscarinic receptor pathways, and that antagonizing the function of IL-1β has a promising future as a potential drug target for asthma treatment. IL-1β can activate NF-κB pathways via Toll-like receptors, and NF-κB will eventually transactivate the genes of cytokines, chemokines, proteins of the complement system, adhesion molecules and immune receptors involved in inflammation. IL-1β can activate eosinophils, which can release major basic protein (MBP) to antagonize the M2 receptors leading to excessive acetylcholine release. Acetylcholine has an effect on M3 receptors, which are related to airway smooth muscle contraction and mucus production. IL-1β is reported to activate COX-2 resulting in heterologous desensitization of adenylate cyclase and impairs relaxation of the ASM. IL-1β is involved in mediation of neutrophilic inflammation. Identification of the prominent role of IL-1β in asthma could lead to successful use of anti-IL1β agents.
authors.affiliation: Department of Gynecology and Obstetrics, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, China.
authors.forename: Zhi
authors.initials: Z
authors.lastname: Liao
authors.forename: Hong-tao
authors.initials: HT
authors.lastname: Xiao
authors.forename: Yuan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Rong-Sheng
authors.initials: RS
authors.lastname: Tong
authors.forename: Li-Juan
authors.initials: LJ
authors.lastname: Zhang
authors.forename: Yuan
authors.initials: Y
authors.lastname: Bian
authors.forename: Xia
authors.initials: X
authors.lastname: He
mesh_terms: D001249:Asthma / Q000378:metabolism* / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism*; D009119:Muscle Contraction / Q000502:physiology; D009130:Muscle, Smooth / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D053583:Interleukin-1beta
keywords: IL-1β; asthma; hyperreactivity; muscarinic receptors; toll-like receptor