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Human recombinant interleukin-1 beta induces thromboxane A2 release in polymorphonuclear leukocytes, macrophages and
M Reale1, R C Barbacane, S Frydas
1Immunology Division, Medical School, University of Thessaloniki, Greece.
Abstract:
Prostaglandins and thromboxanes (Txs) are produced by polymorphonuclears (PMNs) and macrophages (Mphis) in response to various stimuli. PMNs were separated from other human blood cells and Mphis 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 (TxB2) by PMNs and Mphis. 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 TxB2 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-1 beta stimulates TxB2 release in PMNs, Mphis 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-1ra) 500 ng/ml for 10 min and then treated with LPS or hrIL-1 beta 10 micrograms/ml, the release of TxB2 was partially inhibited. IL-1ra may play a significant role in the control of IL-1 and LPS induction in the release of TxB2.
Insights
Human recombinant interleukin-1 (hrIL-1) stimulates thromboxane B2 release in immune cells and platelets, with calcium enhancing this effect. Interleukin-1 receptor antagonist partially inhibits this release, suggesting its role in regulating thromboxane production.
Area of Science:
- Immunology
- Biochemistry
- Cell Biology
Background:
- Prostaglandins and thromboxanes (Txs) are key inflammatory mediators produced by polymorphonuclear leukocytes (PMNs) and macrophages (Mphis).
- Interleukin-1 (IL-1) is a critical cytokine involved in immune responses and inflammation.
Purpose of the Study:
- To investigate the effect of human recombinant interleukin-1 (hrIL-1) on thromboxane B2 (TxB2) release and cellular aggregation in PMNs, macrophages, and platelets.
- To explore the role of calcium ions and IL-1 receptor antagonist (IL-1ra) in modulating these processes.
Main Methods:
- Isolation of human PMNs and rat Mphis.
- Stimulation of isolated cells and human platelets with hrIL-1, calcium ions, and lipopolysaccharide (LPS).
- Measurement of TxB2 release and assessment of cellular aggregation using various experimental conditions.
Main Results:
- hrIL-1 significantly stimulates TxB2 release from PMNs, Mphis, and human platelets.
- Calcium ions (7 mM) potentiate hrIL-1-induced TxB2 release and cause minor aggregation of PMNs when combined with hrIL-1.
- hrIL-1 induces reversible aggregation of platelets at 100 ng/ml.
- IL-1ra partially inhibits hrIL-1 and LPS-induced TxB2 release in monocytes.
Conclusions:
- hrIL-1 beta is a potent stimulator of TxB2 release in PMNs, Mphis, and platelets, an effect amplified by calcium ions.
- IL-1ra plays a role in controlling IL-1 and LPS-induced TxB2 release, highlighting its potential regulatory function in inflammatory pathways.