Abstract
The encounter of neutrophils with immune complexes and complement components — in the bulk phase or on a surface — leads to their secretion of lysosomal hydrolases, especially neutral proteases, which provoke tissue injury. Secretion of lysosomal enzymes and generation of reactive oxygen species (e.g., O2 p2212; generation are stimulus-specific and can be dissected to establish cause and effect relationships by means of: a) kinetic analysis, b) variations in the stimulus, and c) use of impermeant reagents to block discrete responses. Neutrophils also generate products of 11-cyclooxygenase (e.g., PGE2, TxA2) and of the 5- and 15-lipoxygenases (mono-, di-, and tri-HETEs, LTB4, and their isomers). But the cyclooxygenase products (save TxA2) are not phlogistic by themselves: they inhibit the functions of neutrophils, platelets, macrophages, and mast cells. The most potent pro-inflammatory agent yet identified as a product of arachidonate is LTB4. LTB4 is a potent Ca ionophore, constricts airways, is a potent chemoattractant, and induces local inflammation.
Recipient of Predoctoral Fellowship CAO-9161, Department of Pathology, New York University School of Medicine
Fellows of the Arthritis Foundation
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Weissmann, G., Serhan, C., Korchak, H.M., Smolen, J.E. (1984). Mechanisms of Mediator Release from Neutrophils. In: Acton, R.T., Daniel Lynn, J. (eds) Eukaryotic Cell Cultures. Advances in Experimental Medicine and Biology, vol 172. Springer, New York, NY. https://doi.org/10.1007/978-1-4615-9376-8_29
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