NEUTROPHILS: RELEASE OF MEDIATORS OF INFLAMMATION WITH SPECIAL REFERENCE TO RHEUMATOID ARTHRITIS*

作者: Gerald Weissmann , Charles Serhan , Helen M. Korchak , James E. Smolen

DOI: 10.1111/J.1749-6632.1982.TB22122.X

关键词:

摘要: The encounter of neutrophils with immune complexes and complement components, in the bulk phase or on a surface, leads to their secretion lysosomal hydrolases, especially neutral proteases, which provoke tissue injury. Secretion enzymes generation reactive oxygen species (e.g., O(2)) is part stimulus-secretion response variety secretagogues, including components. However, pathways O(2) are stimulus-specific can be dissected establish cause effect relationships by means of: a) kinetic analysis, b) variations stimulus, c) use impermeant reagents block discrete responses. Neutrophils also generate products 11-cyclooxygenase PGE2, TxA2) 5-and 15-lipoxygenases (mono-, di-, tri-HETEs, LTB4, isomers). But cyclooxygenase (save not phlogistic themselves: they inhibit functions neutrophils, platelets, macrophages, mast cells. most potent pro-inflammatory agent yet identified as product arachidonate LTB4. LTB4 Ca ionophore, constricts airways, chemoattractant, induces local inflammation.

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