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   <subfield code="a">Human recombinant interleukin-1β induces thromboxane A2 release in polymorphonuclear leukocytes, macrophages and platelets: Effect of IL-1 receptor antagonist</subfield>
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   <subfield code="c">[M. Reale, R. Barbacane, S. Frydas, G. Anogianakis, A. Trakatellis, D. Dimitriadou, D. Vacalis, F. Placido, P. De Fazio, E. Porreca, C. Di Febbo, P. Conti]</subfield>
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   <subfield code="a">Prostaglandins and thromboxanes (T×s) are produced by polymorphonuclears (PMNs) and macrophages (MØs) in response to various stimuli. PMNs were separated from other human blood cells and MOs were separated from rat peritoneal lavage. In this paper we show that human recombinant interleukin-1 (hrIL-1) can stimulate the release of thromboxane B2(T×B2) by PMNs and MØs. In addition, we have shown that aggregation of PMNs may occur when calcium ions (7 mM) and hrIL-1 (100 ng/ml) are added to the cell preparation, but not when Ca2+ alone, hrIL-1 alone, or first hrIL-1 then calcium are added to the cell preparation. The treatment of human platelets with hrIL-1 shows that after 15 min incubation T×B2 is released. In addition, we compared the aggregation of platelets caused by ADP with that caused by hrIL-1. Human recombinant IL-1 at a concentration of 100 ng/ml also causes little aggregation of platelets, in this case the aggregation is reversible. In conclusion, hrIL-1β stimulates T×B2 release in PMNs, MØs and platelets and this effect increases with addition of Ca2+ ions. The mixture of hrIL-1 and Ca2+ causes little aggregation of PMNs. In monocyte suspensions, pretreated with human recombinant IL-1 receptor antagonist (IL-Ira) 500 ng/ml for 10 min and then treated with LPS or hrIL-1β 10 μg/ml, the release of T×B2 was partially inhibited. IL-Ira may play a significant role in the control of IL-1 and LPS induction in the release of T×B2.</subfield>
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