Abstract
BackgroundCigarette smoking induces peripheral inflammatory responses in all smokers and is the major risk factor for neutrophilic lung disease such as chronic obstructive pulmonary disease. The aim of this study was to investigate the effect of cigarette smoke on neutrophil migration and on β2-integrin activation and function in neutrophilic transmigration through endothelium.Methods and resultsUtilizing freshly isolated human PMNs, the effect of cigarette smoke on migration and β2-integrin activation and function in neutrophilic transmigration was studied. In this report, we demonstrated that cigarette smoke extract (CSE) dose dependently induced migration of neutrophils in vitro. Moreover, CSE promoted neutrophil adherence to fibrinogen. Using functional blocking antibodies against CD11b and CD18, it was demonstrated that Mac-1 (CD11b/CD18) is responsible for the cigarette smoke-induced firm adhesion of neutrophils to fibrinogen. Furthermore, neutrophils transmigrated through endothelium by cigarette smoke due to the activation of β2-integrins, since pre-incubation of neutrophils with functional blocking antibodies against CD11b and CD18 attenuated this transmigration.ConclusionThis is the first study to describe that cigarette smoke extract induces a direct migratory effect on neutrophils and that CSE is an activator of β2-integrins on the cell surface. Blocking this activation of β2-integrins might be an important target in cigarette smoke induced neutrophilic diseases.
Highlights
Cigarette smoking induces peripheral inflammatory responses in all smokers and is the major risk factor for neutrophilic lung disease such as chronic obstructive pulmonary disease
This is the first study to describe that cigarette smoke extract induces a direct migratory effect on neutrophils and that CSE is an activator of b2-integrins on the cell surface
Blocking this activation of b2-integrins might be an important target in cigarette smoke induced neutrophilic diseases
Summary
Cigarette smoking induces peripheral inflammatory responses in all smokers and is the major risk factor for neutrophilic lung disease such as chronic obstructive pulmonary disease. Neutrophils play a pivotal role in pulmonary inflammatory diseases, such as chronic obstructive pulmonary disease (COPD). COPD is a progressive disease, which is characterized by two major pathological processes, namely bronchitis and emphysema. The neutrophils accumulate in the affected tissues and contribute to the chronic inflammatory reaction, eventually leading to lung destruction [1,2]. It is generally accepted that cigarette smoking is the most important risk factor for the development of COPD. COPD patients have increased neutrophil counts in bronchoalveolar lavage fluid (BALF) and sputum [4,5,6,7]; increased neutrophil numbers are
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