The inflammatory response in lung tissue is an important part of host defense that aids in removing microorganisms or particles that have reached the distal airways and alveolar surface. It augments the usual function of alveolar macrophages, immunoglobulins, and other defense mechanisms such as mucociliary clearance. However, excessive or poorly regulated inflammation can be destructive of tissue, thus contributing to many disease processes that can lead to fibrosis and impaired gas exchange. Several examples of diseases that feature inflammation as part of their pathophysiology have been selected for this review; i.e. asthma (especially examining the late-phase reaction that involves PMNs), chronic bronchitis (in which irritants and bacterial products may stimulate mucus secretion and inflammatory cells), interstitial lung diseases (IPF may disclose PMNs but sarcoidosis and hypersensitivity pneumonitis feature collections of activated lymphocytes), and acute lung injury leading to adult respiratory distress syndrome (PMNs and their breakdown products and enzymes incite local destruction of alveolar tissue). In preparation for these disease examples, a thorough review of the normal interactions between alveolar macrophages, various opsonins, complement and chemotactic factors, and the responsiveness of PMNs is given first.