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Phenolic glycolipid-1 from M. leprae inhibits oxygen free radical production by human mononuclear cells.
Research in Immunology
We studied the effect of PGL1, a phenolic glycolipid unique to Mycobacterium leprae, on the activation of the phagocyte oxidative respiratory burst, by measuring the chemiluminescence (CL) generated by normal mononuclear cells. PGL1 induced a decrease in oxygen free radical production stimulated by mycobacteria (M. leprae, BCG and M. kansasii) or by phorbol myristate acetate, but did not prevent the binding or ingestion of fluorescein-conjugated mycobacteria. In contrast, mycoside A from M. kansasii, a structurally related compound, did not alter the CL response. In addition, treatment of M. leprae with anti-PGL1 antibodies failed to restore the response to this microorganism. PGL1 could act as an oxygen species scavenger and protect M. leprae from killing by toxic oxygen metabolites.
Adult, Antibodies, Bacterial/pharmacology, Antigens, Bacterial, Free Radicals, Glycolipids/immunology, Glycolipids/pharmacology, Humans, Leukocytes, Mononuclear/drug effects, Leukocytes, Mononuclear/immunology, Luminescent Measurements, Mycobacterium/immunology, Mycobacterium bovis/immunology, Mycobacterium leprae/immunology, Oxygen/blood, Phagocytosis/drug effects, Tetradecanoylphorbol Acetate/pharmacology
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