Mechanisms of mediator release from neutrophils.
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-. 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.
D000527:Alprostadil; D000936:Antigen-Antibody Complex / Q000276:immunology*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000097:blood; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D000242:Cyclic AMP / Q000097:blood; D006801:Humans; D006867:Hydrolases / Q000378:metabolism; D007700:Kinetics; D008247:Lysosomes / Q000201:enzymology; D008563:Membrane Lipids / Q000097:blood; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D010743:Phospholipids / Q000097:blood; D011458:Prostaglandins E / Q000494:pharmacology
D000936:Antigen-Antibody Complex; D001095:Arachidonic Acids; D008563:Membrane Lipids; D010743:Phospholipids; D011458:Prostaglandins E; D016718:Arachidonic Acid; D009240:N-Formylmethionine Leucyl-Phenylalanine; D000242:Cyclic AMP; D006867:Hydrolases; D000527:Alprostadil