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

Respiratory Research

Reynold A Panettieri¹  Hang Chen¹  Yassine Amrani¹ 

[1] University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, USA

关键词: thapsigargin;    tumor necrosis factor receptor 1;    tumor necrosis factor-α;    airway smooth muscle;    airway remodeling;    airway hyper-responsiveness;   

Others  :  1227494
DOI  :  10.1186/rr12

 received in 2000-06-07, accepted in 2000-06-13,  发布年份 2000

【 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.

【 授权许可】

   
2000 Current Science Ltd

【 图 表 】

Figure 1.

Figure 2.

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