The Role of PMN-Leukocyte Lysosomes in Tissue Injury, Inflammation and Hypersensitivity

Prostaglandins and leucotaxis

“…They not only enhance the impaired vascular permeability by potentiating the effects of other mediators (Moncada, Ferreira & Vane, 1973;Williams & Morley, 1973) but could sustain the inflammatory reaction by acting as leucotactic factors (Kaley & Weiner, 1971a). It has been proposed that the main source of the prostaglandins in the later phases of immunogenic uveitis, carrageenan-induced pleurisy and various paw oedemas is the polymorphonuclear leucocyte which releases E-type prostaglandins during phagocytosis (Movat, Macmorine & Takeuchi, 1971 ;Eakins, Whitelocke & others, 1972;Higgs & Youlten, 1972). The anti-inflammatory actions of conventional non-steroidal acidic anti-inflammatory drugs, such as aspirin, phenybutazone and indomethacin, become explicable on the basis of a primary interference with the biosynthesis of PGs in vivo (Vane, 1973).…”

Neutropenia induced by platelet-activating factor (PAF-acether) released from neutrophils: The inhibitory effect of prostacyclin (PGI2)

“…The release of PAF acether from PMN (1 • 106/ml Tris Tyrode's buffer with 0.25% bovine serum albumin: TT BSA) stimulated with C5a (0.2 ~g/ml), C5adesArg (0.2 l~g/ml) and C BYS (1 • 107/ml) seems to be a two step process of membrane phospholipid activation involving the membrane phospho lipase A 2 in the release of 2 Lyso PAF, as inferred by inhibition (75%) of PAFacether release by bromo diphenacylbromide (1 x 10 6 M; PBDB), and the subsequent acetylation in position 2, as suggested by the marked increase in PAF-acether (150%) yield in the presence of sodium acetate (1 x 10 3 M). PMN (1 x 106/ml TT BSA), preincubated (20 min at 22~ in the presence of 200 ~Ci/ml of 14CH3COONa (50 mCi/mM) and stimulated with 1 x 10V/ml C BYS incorporate 14CH3COOH into the released PAF acether, a fact consistent with the importance of an acetylation process as described elsewhere for platelets [161. PAF , the PMN bind PAF-acether to a greater extent than lymphocytes and erythrocytes and the cell surface area requirements for PAF-acether binding to PMN are similar to those for platelets [20,21 ].…”

The Pharmacological Mediation of the Acute Inflammatory Response: A Brief Review*

“…The source of the prostaglandins is unknown, but there is some evidence that leucocytes, possible macrophages, are required, for tlieir release (Higgs and Youlton, 1972 ;Movat et al, 1971 ;Velo et al, 1973). In addition to these cells, the complement system is involved in prostaglandin jn'oduction and release (Willoughby and Di Rosa, 1971).…”