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- W2132450798 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., O(2)) is part of a stimulus-secretion response to a variety of secretagogues, including immune complexes and complement components. However, the pathways of secretion and O(2) 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." @default.
- W2132450798 created "2016-06-24" @default.
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- W2132450798 date "1982-06-01" @default.
- W2132450798 modified "2023-10-18" @default.
- W2132450798 title "NEUTROPHILS: RELEASE OF MEDIATORS OF INFLAMMATION WITH SPECIAL REFERENCE TO RHEUMATOID ARTHRITIS" @default.
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- W2132450798 doi "https://doi.org/10.1111/j.1749-6632.1982.tb22122.x" @default.
- W2132450798 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/6807175" @default.
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