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Updated: Oct 3, 2026

In vitro Measurements of Tracheal Constriction Using Mice
Published on: June 25, 2012
Activation of tumor necrosis factor receptor 1 in airway smooth muscle: a potential pathway that modulates bronchial
Y Amrani1, H Chen, R A Panettieri
1Pulmonary, Allergy and Critical Care Division, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104-6160, USA. amrani@mail.med.upenn.edu
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.
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