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

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: " Activation of tumor necrosis factor receptor 1 in airway smooth muscle: a potential pathway that modulates bronchial hyper-responsiveness in asthma. | http respiratory-research.eom content 1 1 049 Review 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 and Reynold A Panettieri Jr University of Pennsylvania Medical Center Philadelphia Pennsylvania USA Received 7 June 2000 Accepted 13 June 2000 Published 3 July 2000 Respir Res 2000 1 49-53 Current Science Ltd Print ISSN 1465-9921 Online ISSN 1465-993X Abstract The cellular and molecular mechanisms that are involved in airway hyper-responsiveness are unclear. Current studies suggest that tumor necrosis factor TNF -a 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-a 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-KB NF-kB pathway alters calcium homeostasis in ASM which appears to be a new potential mechanism underlying ASM hyper-responsiveness. 5 Keywords airway hyper-responsiveness airway remodeling airway smooth muscle tumor necrosis factor-a tumor necrosis factor receptor 1 thapsigargin Introduction Asthma which is characterized by airway inflammation exaggerated airway reactivity to contractile agonists and a decrease in p-adrenoceptor-mediated airway relaxation remains a common cause of pulmonary morbidity and mortality. Although the mechanisms that underlie changes in airway responsiveness are unknown recent reports support the notion that inflammatory mediators which are present in high levels in asthmatic airways directly modulate ASM function. Using cultured human ASM cells that retain .