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.