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:"Autocrine regulation of asthmatic airway inflammation: role of airway smooth muscle. | Available online http content 3 1 11 Review Autocrine regulation of asthmatic airway inflammation role of airway smooth muscle Sue McKay and Hari S Sharma Department of Pharmacology Erasmus University Medical Centre Rotterdam The Netherlands Correspondence Hari S Sharma MPhil PhD Cardiopulmonary and Molecular Biology Laboratory Institute of Pharmacology Erasmus University Medical Center Dr Molewaterplein 50 3015 GE Rotterdam The Netherlands. Tel 31 10 4087963 fax 31 10 408 9458 e-mail sharma@ Received 26 March 2001 Revisions requested 3 May 2001 Revisions received 18 October 2001 Accepted 23 October 2001 Published 28 November 2001 Respir Res 2002 3 11 2002 BioMed Central Ltd Print ISSN 1465-9921 Online ISSN 1465-993X Abstract Chronic airway inflammation is one of the main features of asthma. Release of mediators from infiltrating inflammatory cells in the airway mucosa has been proposed to contribute directly or indirectly to changes in airway structure and function. The airway smooth muscle which has been regarded as a contractile component of the airways responding to various mediators and neurotransmitters has recently been recognised as a rich source of pro-inflammatory cytokines chemokines and growth factors. In this review we discuss the role of airway smooth muscle cells in the regulation and perpetuation of airway inflammation that contribute to the pathogenesis of asthma. Keywords airway smooth muscle chemokine cytokine growth factor inflammation Introduction Inflammation of the airway wall is a central characteristic of asthma 1 . Airborne allergens often lead to an accumulation of eosinophils lymphocytes predominantly CD4 type mast cells and macrophages resulting in an inflammatory reaction in the mucosa. Neutrophil numbers can increase during an exacerbation. The release of mediators from these inflammatory cells has been proposed to contribute directly or indirectly to changes in airway structure and function. .
