Induction of superoxide anion production from monocytes and neutrophils by activated platelets through the P-selectin–sialyl Lewis X interaction

Abstract

Activated platelets expressing P-selectin on their surface are known to adhere to monocytes and neutrophils. We examined the possibility that the leukocytes were activated by their adhesion to activated platelets and demonstrated that P-selectin-dependent platelet adhesion to neutrophils and monocytes induced production of extracellular superoxide anion (O2-) by these leukocytes. Leukocyte membrane glycoproteins containing Ser/Thr-linked carbohydrate chains were responsible for the signal reception leading to the leukocyte activation. Cytokines were shown to influence these processes. For example, treatments of neutrophils with interleukin-8 (IL-8) or granulocyte colony-stimulating factor (G-CSF) potentiated the P-selectin-induced O2- production. Furthermore, interleukin-1 (IL-1) and interferon-gamma (IFN-gamma) induced surface expression of P-selectin on platelets in the presence of a low concentration of thrombin and consequently enhanced their adhesion capacity to leukocytes. These results indicated that the adhesion of activated platelets to the leukocytes through the interaction between P-selectin and its carbohydrate ligand, sialyl Lewis X (LeX), was a crucial step for the activation of leukocyte function and supported the notion that activated platelets were actively involved in the inflammatory processes.

Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

“…Consequently, the CL-response effect of anti-PSGL-1 was especially potent under stirring conditions. Furthermore, Tsuji et al demonstrated that thrombin-activated platelets enhanced the extracellular release of superoxide anion from neutrophils via P-selectin interaction with sialyl Lewis X [47]. They also noticed, in accordance with Wong et al and the present study, that soluble recombinant P-selectin rather inhibited than potentiated the effects on the neutrophil respiratory burst [47,48].…”

“…Furthermore, Tsuji et al demonstrated that thrombin-activated platelets enhanced the extracellular release of superoxide anion from neutrophils via P-selectin interaction with sialyl Lewis X [47]. They also noticed, in accordance with Wong et al and the present study, that soluble recombinant P-selectin rather inhibited than potentiated the effects on the neutrophil respiratory burst [47,48]. This is probably due to that isolated platelet P-selectin is dimeric, both in -granules of resting cells and on activated platelet surfaces [49].…”

Granulocyte colony-stimulating factor (G-CSF) transiently suppresses mitogen-stimulated T-cell proliferative response

“…It is known that oxidative stress favours both apoptosis and anergy of T lymphocytes (Buttke and Sandstrom, 1994) and that G-CSF enhances superoxide production by mature neutrophils (Tsuji et al, 1994). The effects of the superoxide production induced by G-CSF treatment on the T lymphocyte functions remain to be defined.…”

P-selectin and MAC-1 mediate monocyte rolling and adhesion to ECM-bound platelets under flow conditions

“…It is tempting to speculate that monocyte activation takes place during the tethering and initial interaction with platelets, leading to a high-affinity state of integrins for their ligands. In support of this concept is the finding that binding of P-selectin or activated platelets to monocytes induces intracellular signaling and activation [39][40][41].…”