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Title: Activation of tumor necrosis factor receptor 1 in airway smooth muscle: a potential pathway that modulates bronchial hyper-responsiveness in asthma?
Authors: Amrani, Yassine
Chen, H.
Panettieri, R. A.
First Published: 3-Jul-2000
Publisher: BioMed Central
Citation: Respiratory Research, 2000, 1 (1), pp. 49-53
Abstract: The cellular and molecular mechanisms that are involved in airway hyper-responsiveness are unclear. Current studies suggest that tumor necrosis factor (TNF)-alpha, a cytokine that is produced in considerable quantities in asthmatic airways, may potentially be involved in the development of bronchial hyper-responsiveness by directly altering the contractile properties of the airway smooth muscle (ASM). The underlying mechanisms are not known, but growing evidence now suggests that most of the biologic effects of TNF-alpha on ASM are mediated by the p55 receptor or tumor necrosis factor receptor (TNFR)1. In addition, activation of TNFR1 coupled to the tumor necrosis factor receptor-associated factor (TRAF)2-nuclear factor-kappaB (NF-kappaB) pathway alters calcium homeostasis in ASM, which appears to be a new potential mechanism underlying ASM hyper-responsiveness.
DOI Link: 10.1186/rr12
ISSN: 1465-9921
eISSN: 1465-993X
Type: Journal Article
Rights: © 2000 Current Science Ltd. Creative Commons Attribution License 4.0. (CC BY 4.0) (
Description: PMCID: PMC59542
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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