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Objective:To investigate the role of macrophage inflammatory protein-1alpha(MIP-1 alpha) in the detrimental enhancement of matrix mnetalloproteinase-9(MMP-9) expression,release and activity induced by phagocytosis of malarial pigment(haemozoin,HZ) in human monocytes. Methods:Human adherent monocytes were unfed/fed with native HZ for 2 h.After 24 hours. MIP-1 alpha production was evaluated by ELISA in cell supernatants.Alternatively.HZunfed /fed monocytes were treated in presence/absence of anti-human MIP-1 alpha blocking antibodies or recombinant human MIP-lalpha for 15 h(RNA studies) or 24 h(protein studies): therefore,MMP-9 mRNA expression was evaluated in cell lysatcs by Real Time RT-PCR,whereas proMMP-9 and active MMP-9 protein release were measured in cell supernatants by Western blotting and gelatin zvmography.Results:Phagocytosis of HZ by human monocytes increased production of MIP-1 alpha.mRNA expression of MMP-9 and protein release of proMMP-9 and active MMP-9.All the HZ-enbancing effects on MMP-9 were abrogated by anti-human MIP- 1 alpha blocking antibodies and mimicked by recombinant human MIP-l alpha.Conclusions: The present work suggests a role for MIP-lalpha in the HZ-dependent enhancement of MMP-9 expression,release and activity observed in human monocytes.higbligbtiug new detrimental effects of HZ-triggered proinflammatory response by phagocytic cells in falciparum malaria.
Objective: To investigate the role of macrophage inflammatory protein-1alpha (MIP-1 alpha) in the detrimental enhancement of matrix mnetalloproteinase-9 (MMP-9) expression, release and activity induced by phagocytosis of malarial pigment (haemozoin, HZ) Monocytes. Methods: Human adherent monocytes were unfed / fed with native HZ for 2 h. After 24 hours. MIP-1 alpha production was evaluated by ELISA in cell supernatants. Alternatively. Hff / fed monocytes were treated in presence / absence of anti- human MIP-1 alpha blocking antibodies or recombinant human MIP-lalpha for 15 h (RNA studies) or 24 h (protein studies): therefore, MMP-9 mRNA expression was evaluated in cell lysatcs by Real Time RT- 9 and active MMP-9 protein release were measured in cell supernatants by Western blotting and gelatin zvmography. Results: Phagocytosis of HZ by human monocytes increased production of MIP-1 alpha. MRNA expression of MMP-9 and protein release of proMMP-9 and active MMP-9.All the HZ-enban cing effects on MMP-9 were abrogated by anti-human MIP-1 alpha blocking antibodies and mimicked by recombinant human MIP-1 alpha. Conclusions: The present work suggests a role for MIP-lalpha in the HZ-dependent enhancement of MMP-9 expression, release and activity observed in human monocytes. Hgbligbtiug new detrimental effects of HZ-triggered proinflammatory response by phagocytic cells in falciparum malaria.