Mechanisms by which leukocytes emigrate and induce tissue destruction

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Abstract
Chronic inflammatory reactions are characterized by emigration of leukocytes to chemotactic stimuli and the subsequent release of intracellular enzymes which propogate the imflammatory reaction and causes tissue injury. The adoptive transfer of isologous51Cr labeled leukocytes was used as a model to dissect the cellular mechanisms involved in cell accumulation to the site of immune complex or complement mediated imflammatory reactions. An intact microtubular system was necessary only for neutrophil emigration whereas cell membrane integrity was necessary for mononuclear cell but not neutrophil accumulation in vivo. The accumulation of both cell types was inhibited following phagocytosis or in the presence of corticosteroids. Release of protein polysaccharide degrading neutral protease activity from leukocytes in the presence of immune complexes was dependant upon intact microtubular activity and cell membrane integrity since agents affecting these systems inhibited enzyme release. Conversely collagenase activity released from leukocytes under the same conditions was not inhibited by these agents. Evidence will be presented indicating that the emigration of specific cell types and the release of selected enzyme systems are controlled by separate and distinct mechanistic pathways.