Abstract
Several lines of evidence suggest that the imbalance of the humoral-phagocytic immune system conclusively contributes to the development of the adult respiratory distress syndrome (ARDS) [16, 19, 35]. Furthermore, polymorphonuclear leukocytes (PMNLs) are believed to play an essential role in the initiation and amplification of the lung tissue injury processes leading to increased lung permeability and the onset of ARDS. After being stimulated intravascularly, neutrophils adhere to the capillary endothelium, especially of the lung, and then pass across the capillary-interstitial-alveolar space while releasing inflammatory mediators such as arachidonic acid metabolites, oxygen-derived agents, and lysosomal enzymes [26, 29, 33]. These release reactions are coupled to stimulatory response mechanisihs in which soluble and/or particulate stimulators cause extracellular release of respiratory burst products and lysosomal enzymes which lead to an increase in photon emission [1].
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