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

Yassine Amrani, Hang Chen, Reynold A. Panettieri

Research output: Contribution to journalArticlepeer-review

102 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)49-53
Number of pages5
JournalRespiratory Research
Volume1
Issue number1
DOIs
StatePublished - 2000

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Keywords

  • Airway hyper-responsiveness
  • Airway remodeling
  • Airway smooth muscle
  • Thapsigargin
  • Tumor necrosis factor receptor 1
  • Tumor necrosis factor-α

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