Báo cáo y học: " Role of the tachykinin NK1 receptor in a murine model of cigarette smoke-induced pulmonary inflammation"

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: " Role of the tachykinin NK1 receptor in a murine model of cigarette smoke-induced pulmonary inflammation. | Respiratory Research BioMed Central Research Role of the tachykinin NK1 receptor in a murine model of cigarette smoke-induced pulmonary inflammation Katelijne O De Swert Ken R Bracke Tine Demoor Guy G Brusselle and Guy F Joos Open Access Address Laboratory for Translational Research in Obstructive Pulmonary Diseases Department of Respiratory Medicine Ghent University Hospital Ghent Belgium Email Katelijne O De Swert - kdswert@ Ken R Bracke - Tine Demoor - Guy G Brusselle - Guy F Joos - Corresponding author Published 15 May 2009 Received 6 March 2009 Respiratory Research 2009 10 37 doi l465-992l-l0-37 Accepted 15 May 2009 This article is available from http content l0 l 37 2009 De Swert et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background The tachykinins substance P and neurokinin A present in sensory nerves and inflammatory cells such as macrophages and dendritic cells are considered as pro-inflammatory agents. Inflammation of the airways and lung parenchyma plays a major role in the pathogenesis of chronic obstructive pulmonary disease COPD and increased tachykinin levels are recovered from the airways of COPD patients. The aim of our study was to clarify the involvement of the tachykinin NKl receptor the preferential receptor for substance P in cigarette smoke CS -induced pulmonary inflammation and emphysema in a mouse model of COPD. Methods Tachykinin NK1 receptor knockout NK1-R- - mice and their wild type controls all in a mixed l29 sv-C57BL 6 background were subjected to sub acute 4 weeks or chronic 24 weeks exposure to air or CS. 24 hours after the last exposure pulmonary

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