Reduction in Neutrophil Cell Surface Expression of Tumor Necrosis Factor Receptors but Not Fas After Transmigration

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Abstract
THE STUDY of neutrophil apoptosis has been stimulated by the belief that neutrophils are implicated in the pathogenesis of persistent inflammatory states, including multiple organ dysfunction syndrome and adult respiratory distress syndrome. Neutrophils possess a variety of means of inducing tissue injury,1 including the secretion of connective-tissue proteases capable of tissue destruction in septic shock.2 There is an association between neutrophil number and level of activation and the degree of inflammation,3 as well as pulmonary vascular permeability,4 in patients with adult respiratory distress syndrome. Prevention of neutrophil sequestration will lead to reduced tissue injury in multiple animal models.5-7 In addition, clearance of neutrophils is associated with resolution of inflammation.8 Neutrophil apoptosis, a genetically programmed form of cell death fundamentally distinct from necrosis, is the principal mode by which senescent neutrophils are cleared from circulation.9 It has been suggested that an imbalance of granulocyte apoptosis and necrosis may be important in the pathogenesis of inflammatory disease.10 Thus, the study of neutrophil apoptosis is vital to better understand the persistent inflammation common to patients with multiple organ dysfunction syndrome and adult respiratory distress syndrome.

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