Local and systemic cellular inflammation and cytokine release in chronic obstructive pulmonary disease

Background: Chronic obstructive pulmonary disease (COPD) is a chronic airway inflammatory disease caused by repeated exposure to noxious gases or particles. It is now recognized that the disease also features systemic inflammation. The purpose of our study was to compare airway and systemic inflammation in COPD to that seen in healthy subjects and to relate the inflammation with the disease severity. Methods: Ninety-five COPD patients, encompassing the whole severity spectrum of the disease, were recruited from our outpatient clinic and rehabilitation center and compared to 33 healthy subjects. Induced sputum and blood samples were obtained for measurement of inflammatory cell count. Interleukin (IL)-4, IL-6, IL-10, TNF-alpha and IFN-gamma produced by 24 h sputum and blood cell cultures were measured. Results: Compared to healthy subjects, COPD exhibited a prominent airway neutrophilic inflammation associated with a marked IL-10, IL-6 and TNF-alpha release deficiency that contrasted with a raised IFN-gamma production. Neutrophilic inflammation was also prominent at blood level together with raised production of IFN-gamma, IL-10 and TNF-alpha. Furthermore, sputum neutrophilia correlated with disease severity assessed by GOLD stages. Likewise the extent of TNF-alpha release from blood cells also positively correlated with the disease severity but negatively with that of sputum cell culture. Blood release of TNF-alpha and IL-6 negatively correlated with body mass index. Altogether, our results showed a significant relationship between cellular marker in blood and sputum but poor relationship between local and systemic release of cytokines. Conclusions: COPD is characterized by prominent neutrophilic inflammation and raised IFN-gamma production at both bronchial and systemic level. Overproduction of TNF-alpha at systemic level correlates with disease severity and inversely with body mass index. (C) 2011 Elsevier Ltd. All rights reserved.