The aim of this study is to examine the inflammatory mechanisms involved in the pathogenesis of inflammatory lung disease, in particular to compare the inflammatory profile seen in asthma and COPD. Evidence for inflammation in asthma and COPD is based on the finding of increased numbers of macrophages and neutrophils in the lungs and respiratory secretions of these patients. The inflammatory cells produce proteases, as well as, reactive oxidant species resulting in a protease/anti-protease imbalance which favours lung destruction. The aim is to examine the inflammatory mediators released by inflammatory cells (such as, macrophages and lymphocytes) in order to determine whether there are differences between non-smoking subjects, smoking subjects and patients with asthma or COPD. Monocytes are precursors of alveolar macrophages, and both monocytes and neutrophils are recruited to the lung from the blood via the action of specific chemoattractants. We have evidence that in inflammation there are higher levels of these chemoattractants. Therefore these cells might also demonstrate the same changes seen in alveolar macrophages from these patients.

We also aim to assess the role of the macrophage precursor (monocyte) and neutrophils in the blood. We will also assess lymphocyte/monocyte interaction. We will do this as the lymphocyte may be involved in the initial recruitment of inflammatory cells. We will also assess the role of cytokines involved with monocyte/macrophage/neutrophil migration in induced sputum as well as the role of induced sputum in the migration of monocytes and neutrophils into the lung. Our aim is to link the initial changes in blood to the changes causing disease in the lungs. We aim to examine cellular responses in four groups of subjects, namely (i) non-smoking controls, (ii) smokers without clinical evidence of COPD or asthma, (iii) smokers with COPD (iv) asthmatic patients.