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1Pulmonary, Allergy and Critical Care Medicine Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; 2Jiangsu Key Laboratory for Molecular Medical Biotechnology, Life Sciences College, Nanjing Normal University, Nanjing, China; 3Model Animal Research Center, Nanjing University, Nanjing, China; and 4Cardiovascular Research Institute and the Departments of Medicine and Anesthesia, University of California, San Francisco, California
Submitted 4 June 2006 ; accepted in final form 11 January 2007
Cigarette smoking, a major risk factor for chronic obstructive pulmonary disease, can cause airway inflammation, airway narrowing, and loss of elasticity, leading to chronic airflow limitation. In this report, we sought to define the signaling pathways activated by smoke and to identify molecules responsible for cigarette smoke-induced inflammation. We applied cigarette smoke water extract (CSE) to primary human lung fibroblasts and found that CSE significantly increased CXC chemokine IL-8 production. Meanwhile, 70-kDa heat shock protein (HSP70) was also induced by CSE in a dose- and time-dependent manner. CSE treatment stimulated HSP70 secretion by primary fibroblasts, which augmented IL-8 production. This was further confirmed by exogenously added recombinant HSP70. Using HSP70 small interfering RNA, we confirmed that CSE-induced chemokine production was dependent on heat shock protein expression. Further investigation showed that CSE could also stimulate early growth response-1 (EGR-1) in an ERK-dependent manner and that the expression of HSP70 was EGR-1 dependent. In view of these findings, we hypothesize that the MAPK-EGR-1-HSP70 pathway regulates the cigarette smoke-induced inflammatory process.
chronic obstructive pulmonary disease; cigarette smoke extract; early growth response-1; interleukin-8; 70-kDa heat shock protein
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