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Increased activation of p38 MAPK in COPD

¹ Dept of Experimental and Clinical Medicine, University "Magna Græcia" of Catanzaro, Catanzaro, ² Dept of Cardiothoracic and Respiratory Sciences, Second University of Naples, Naples, Depts of ³ Cardiac, Thoracic and Vascular Sciences, and ⁵ Environmental Medicine and Public Health, University of Padova, Padova, ⁴ Dept of Clinical and Experimental Medicine, University of Ferrara, Ferrara, and ⁶ Dept of Oncology, Haematology and Respiratory Disease, University of Modena and Reggio Emilia, Modena, Italy.

CORRESPONDENCE: M. Saetta, Dept of Cardiac, Thoracic and Vascular Sciences, Section of Respiratory Diseases, University of Padova, via Giustiniani 3, Padova, Italy. Fax: 39 0498213110. E-mail: marina.saetta{at}unipd.it

Keywords: Airflow limitation, chronic obstructive pulmonary disease, cigarette smoking, phospho-p38 mitogen-activated protein kinases

Received: March 27, 2007
Accepted October 16, 2007

Inflammation, oxidative stress and apoptosis, which are involved in chronic obstructive pulmonary disease (COPD) pathogenesis, may activate the p38 subgroup of mitogen-activated protein kinases (MAPKs). Therefore, the aim of the present study was to evaluate the expression of the phosphorylated, active form of p38 MAPK (phospho-p38) in the lungs of COPD patients.

Surgical specimens were obtained from 18 smokers with COPD at different stages of disease severity, plus nine smoking and eight nonsmoking subjects with normal lung function. Phospho-p38+ cells were quantified by immunohistochemistry in both alveolar spaces and alveolar walls. Moreover, a Western blot analysis of phospho-p38 and total p38 isoform expressed by alveolar macrophages was performed.

Phospho-p38+ alveolar macrophages and phospho-p38+ cells in alveolar walls were increased in patients with severe and mild/moderate COPD, compared with smoking and nonsmoking controls. Moreover, they were inversely correlated to values of forced expiratory volume in one second (FEV₁) and FEV₁/forced vital capacity. Western blot analysis showed that phosphorylated p38, but not the total p38 isoform, was specifically increased in alveolar macrophages from COPD patients.

Activation of the p38 mitogen-activated protein kinase pathway appears to be involved in the pathogenesis of chronic obstructive pulmonary disease. The present findings suggest that this protein may be a suitable pharmacological target for therapeutic intervention.

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