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Objective:To investigate whether the increase of tumor necrosis factor alpha is dependent on lipidic component of malarial pigment.Methods:Adherent human monocytes were fed for 3 hours with different meals(native hemozoin;lipid free hemozoin;and control latex particles),then tumor necrosis factor alpha was monitored in cell supernatants up to 48 hours through western blotting or specific enzyme-linked immunoadsorbent assay.In selected experiments,unfed monocytes were treated with different doses of 15(S,R)-hydroxy-6,8,11,13-eicosatetraenoic acid or 4-hydroxynonenal instead of phagocytosis.Results:Hemozoin-fed monocytes produced higher levels of tumor necrosis factor alpha than unstimulated and latex-fed cells, while lipid-free hemozoin did not reproduce these results.Additionally,hemozoin effects were mimicked dose-dependently by 15(S,R)-hydroxy-6,8,11,13-eicosatetraenoic acid,but not by 4-hydroxynonenal.Conclusions:Present data suggest an essential role for lipids in hemozoindependent enhanced release of tumor necrosis factor alpha from monocytes,and 15(S,R)hydroxy -6,8,11,13-eicosatetraenoic acid could be one possible specific mediator.
Objective: To investigate whether the increase of tumor necrosis factor alpha is dependent on lipidic component of malarial pigment. Methods: Adherent human monocytes were fed for 3 hours with different meals (native hemozoin; lipid free hemozoin; and control latex particles), then tumor necrosis factor alpha was monitored in cell supernatants up to 48 hours through western blotting or specific enzyme-linked immunoadsorbent assay. In selected experiments, unfed monocytes were treated with different doses of 15 (S, R) -hydroxy-6,8,11, 13-eicosatetraenoic acid or 4-hydroxynonenal instead of phagocytosis. Results: Hemozoin-fed monocytes produced higher levels of tumor necrosis factor alpha than unstimulated and latex-fed cells, while lipid-free hemozoin did not reproduce these results. Additionally, hemozoin effects were mimicked dose-dependently by 15 (S, R) -hydroxy-6,8,11,13-eicosatetraenoic acid, but not by 4-hydroxynonenal. Conclusions: Present data suggest an essential role for lipids in hemozoindependent enhanced release of tumor necrosis factor alpha from monocytes, and 15 (S, R) hydroxy-6,8,11,13-eicosatetraenoic acid could be one possible specific mediator.