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:" Mechanism of cigarette smoke condensate-induced acute inflammatory response in human bronchial epithelial cells. | Available online http content 3 1 22 Research article Mechanism of cigarette smoke condensate-induced acute inflammatory response in human bronchial epithelial cells Gary R Hellermann Szilvia B Nagy Xiaoyuan Kong Richard F Lockey and Shyam S Mohapatra Division of Allergy and Immunology and the Joy McCann Culverhouse Airway Disease Center Department of Internal Medicine University of South Florida College of Medicine and VA Hospital Tampa Florida 3361 2 USA Correspondence Shyam S Mohapatra - smohapat@ Received 6 December 2001 Revisions requested 12 February 2002 Revisions received 11 April 2002 Accepted 8 May 2002 Published 10 July 2002 Respir Res 2002 3 22 2002 Hellerman et al. licensee BioMed Central Ltd Print ISSN 1465-9921 Online ISSN 1465-993X Abstract Background To demonstrate the involvement of tobacco smoking in the pathophysiology of lung disease the responses of pulmonary epithelial cells to cigarette smoke condensate CSC - the particulate fraction of tobacco smoke - were examined. Methods The human alveolar epithelial cell line A549 and normal human bronchial epithelial cells NHBEs were exposed to ig ml CSC a concentration that resulted in 90 cell survival and 5 apoptosis. Changes in gene expression and signaling responses were determined by RT-PCR western blotting and immunocytofluorescence. Results NHBEs exposed to CSC showed increased expression of the inflammatory mediators sICAM-1 IL-1P IL-8 and GM-CSF as determined by RT-PCR. CSC-induced IL-1P expression was reduced by PD98059 a blocker of mitogen-actived protein kinase MAPK kinase MEK and by PDTC a NFkB inhibitor. Analysis of intracellular signaling pathways using antibodies specific for phosphorylated MAPKs extracellular signal-regulated kinase ERK -1 2 demonstrated an increased level of phosphorylated ERK1 2 with increasing CSC concentration. Nuclear localization of phosphorylated ERK1 2 was seen within 30 min of CSC exposure and was inhibited by PD98059. .
