Abstract
The pulmonary vasculature represents the largest reservoir of polymorphonuclear neutrophils (PMNs) in the human body. This is in striking contrast with the paucity of PMNs present in the normal airways and alveoli. However, the respiratory tract constitutes an easy access for microorganisms and particles present in inhaled air and, therefore, efficacious defence mechanisms are required. When the mucociliary clearance and the alveolar macrophages are over-whelmed, the rapid recruitment of PMNs from the lung vasculature appears to be a crucial response of the host against the pathogens. The regulation of adherence of PMNs to endothelial cells (EC), followed by the transendothelial migration are now better understood, and are under the control of a series of adhesion molecules modulated by bacterial and inflammatory mediators. In addition to their defensive role, PMNs have also been implicated in acute and chronic injurious diseases of the lung. Clearly, PMNs contain enough cytotoxic and proteolytic material to induce lesional changes. However, the release of this material is likely to be dependent on environmental factors, including mediators derived from other inflammatory and immune cells. The presence or absence of these factors could explain the fact that high numbers of PMNs can be observed in the airways and alveoli without major lesions whilst in other conditions, a marginal increase of PMNs in the respiratory tract can be associated with major damage and irreversible architectural changes in the lung.
