The fact that the lung stores a large proportion of the marginated pool of neutrophils is a result of the anatomy of the pulmonary microcirculation. This capillary bed is made up of a network of a very large number of segments, many of which have smaller diameters than the neutrophils. Both neutrophils and erythrocytes must deform to pass through the capillary bed, but as the neutrophils are larger and less deformable, they pass through the segments more slowly. The slower movement of neutrophils through the pulmonary capillaries produces little obstruction to erythrocyte flow because the very large number of segments allows the erythrocytes to stream around those that are filled with neutrophils. The size of the marginated pool of neutrophils in the lung depends on the balance between forces that propel the neutrophils through the capillary segments and those that tend to retard them. Activation of the PMN both decreases their deformability and increases their adherence to endothelium, which results in increased numbers of neutrophils in the lung and a reduction in the number circulating in the blood. There is growing evidence that the adherence of the neutrophil to the endothelial cell is mediated by the CD omega 18 on the surface of the neutrophil. The absence of these proteins leads to lack of neutrophil adherence and migration, whereas factors that enhance adherence lead to increased expression of these glycoproteins. The fact that activated neutrophils can also damage normal tissue has led to several attractive hypotheses concerning the pathogenesis of lung diseases such as emphysema and the ARDS. Further elucidation of factors that cause cells to marginate in the pulmonary circulation and a more complete understanding of the factors that control their adherence to endothelium, migration into the interstitial and airspace, and phagocytic function will undoubtedly lead to a better understanding of both the physiology and pathology of the lung.