Activation of tumor necrosis factor receptor 1 in airway smooth muscle: A potential pathway that modulates bronchial hyper-responsiveness in asthma?

被引：108
作者：
Amrani Y. [1 ]
Chen H. [1 ]
Panettieri Jr. R.A. [1 ]
机构：
[1] Pulmonary Allergy/Critical Care Div., Univ. of Pennsylvania Medical Center, Philadelphia, PA 19104-6160
来源：
Respiratory Research | 2000年 / 1卷 / 1期
关键词：
Airway hyper-responsiveness; Airway remodeling; Airway smooth muscle; Thapsigargin; Tumor necrosis factor receptor 1; Tumor necrosis factor-α;
D O I：
10.1186/rr12
中图分类号：
学科分类号：
摘要：
The cellular and molecular mechanisms that are involved in airway hyper-responsiveness are unclear. Current studies suggest that tumor necrosis factor (TNF)-α, 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-α 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-κB (NF-ΚB) pathway alters calcium homeostasis in ASM, which appears to be a new potential mechanism underlying ASM hyper-responsiveness.
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页码：49 / 53
页数：4
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