Abstract
Several lines of evidence suggest that an imbalance of the humoral-phagocytic immune system conclusively contributes to the development of the adult respiratory distress syndrome (ARDS) (Zimmerman 1983; Solomkin 1985; Lanser 1986, Dwenger 1986 a). The most important cells of this system, polymorphonuclear neutrophilic leukocytes (PMNLs), are ambivalent cells in that they manage the host defense by intracellular processing of microorganisms and debris on one hand, and liberate inflammation mediators on the other hand, e.g., by frustrated phagocytosis, thus initiating and enhancing destructive processes in their environment (Dwenger 1986a-c; Regel 1987). After being stimulated intravascularly, neutrophils adhere to the capillary endothelium, preferably in the lung micro-vasculature, and pass across the blood/air barrier into the alveolar space, hereby releasing inflammatory mediators like arachidonic acid metabolites, reactive oxygen agents, and lysosomal enzymes (Worthen 1983), which initiate and/or amplify the destruction of endothelial, interstitial, and epithelial structures (Smedley 1986) and ARDS development.
Supported by the Deutsche Forschungsgemeinschaft, Project II B6.
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References
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© 1989 Springer-Verlag, Berlin Heidelberg
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Dwenger, A., Regel, G., Schweitzer, G., Funck, M., Sturm, J.A., Tscherne, H. (1989). Cellular and Humoral Reactions of the Nonspecific Immune System of Polytraumatized Patients with and without the Adult Respiratory Distress Syndrome. In: Faist, E., Ninnemann, J.L., Green, D.R. (eds) Immune Consequences of Trauma, Shock, and Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73468-7_30
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DOI: https://doi.org/10.1007/978-3-642-73468-7_30
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