Trancellular metabolism of arachidonic acid (AA): Increased platelet thromboxane (TX) generation in the presence of activated polymorphonuclear leukocytes (PMN)

On Radiation Damage to Normal Tissues and its Treatment: II. Anti-inflammatory drugs

“…Singling out the direct endothelial damage by radiation as a primary event is not supported either by the common knowledge that, whereas the microvasculature may be affected, the major blood vessels are mostly spared. Within the narrower scope of this part of the review which focuses on bioactive arachidonic acid dcrivatives, the possibility of blood vessel changes after irradiation being regulatory in character and caused at least in part indirectly (i.e., mediated by diffusible species also generated in nonvascular cells) is further supported by studies on heterologous cell-cell interactions in eicosanoid synthesis (66)(67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77)(78)(79). There seems therefore to be insufficient reason for investigating only the endothelium and vascular smooth muscle cells in an attempt to unravel radiationinduced changes in blood vessels; responses of the intervening (i.e., other stromal and parenchymal) and bloodcirculating cells, as well as reciprocal cell interactions must be taken into account.…”

Clostridium perfringens phospholipase C-induced platelet/leukocyte interactions impede neutrophil diapedesis

“…Neutrophils, however, would retain the ability to bind multiple activated platelets in a rosette pattern. Such interactions are known to hyperstimulate neutrophil respiratory burst activity (Peters et al, 1999;Ruf et al, 1992) and to facilitate chemical cross-talk between these cells, resulting in direct endothelial cell injury and local vascular dysfunction (Ward et al, 1986), and hyperproduction of thromboxanes (Maugeri et al, 1992), leukotrienes (Maugeri et al, 1994) and cytokines (Neumann et al, 1997). Overproduction of these potent immunomodulators could also contribute to local tissue injury and to the systemic manifestations of gas gangrene.…”

Biology and Pathogenesis of Thrombosis and Procoagulant Activity in Invasive Infections Caused by Group A Streptococci andClostridium perfringens

“…Recent studies have demonstrated both the physiologic and pathologic significance of the interaction of activated platelets and leukocytes. As part of the normal inflammatory response, this interaction facilitates the recruitment of PMNL to sites of vascular activation or injury, primes neutrophils for enhanced phagocytosis and killing of foreign microbes (68), enhances monocyte production of cytokines (57), and permits chemical cross talk and signaling between these cell types (33,54). In contrast, these heterotypic cellular complexes also contribute to infectious (19,20) and noninfectious (10, 66; P. A.…”