Activation of tumor necrosis factor receptor 1 in airway smooth muscle- a potential pathway that modulates bronchial hyper-responsiveness in asthma-.pdf (718.3 kB)
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Activation of tumor necrosis factor receptor 1 in airway smooth muscle: a potential pathway that modulates bronchial hyper-responsiveness in asthma?

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journal contribution
posted on 24.10.2012, 09:12 by Yassine Amrani, H. Chen, R. A. Panettieri
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.

Funding

The work of the authors cited in the present review was supported by grants R01-HL64063 and R01-HL55301 from the National Institutes of Health.

History

Citation

Respiratory Research, 2000, 1 (1), pp. 49-53

Published in

Respiratory Research

Publisher

BioMed Central

issn

1465-9921

eissn

1465-993X

Acceptance date

13/06/2000

Copyright date

2000

Available date

24/10/2012

Publisher version

http://www.respiratory-research.com/content/1/1/49

Notes

PMCID: PMC59542

Language

eng