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Suppression of monocyte oxidative response by phenolic glycolipid I of Mycobacterium leprae.

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Abstract Mycobacterium leprae synthesizes a unique phenolic glycolipid (PGL-I) in abundant quantities. We studied the effect of PGL-I on the generation of superoxide anion (O-2) by stimulated human monocytes. Peripheral blood monocytes pretreated with PGL-I released less O-2 when stimulated with M. leprae than did control monocytes. Monocytes pretreated with dimycocerosyl phthiocerol, mycoside A of Mycobacterium kansasii, or mycoside B of Mycobacterium microti, on the other hand, released O-2 in quantities comparable to control monocytes in response to M. leprae stimulation. Monocyte O-2 release in response to other stimuli of the oxidative metabolic burst, such as PMA, zymosan, Mycobacterium bovis Bacille Calmette-Guérin, or M. kansasii, was unaffected by lipid pretreatment. These findings demonstrate that PGL-I has a direct effect on monocyte O-2 generation in response to M. leprae and suggest that PGL-I is a modulator of phagocytic cell function.
Title: Suppression of monocyte oxidative response by phenolic glycolipid I of Mycobacterium leprae.
Description:
Abstract Mycobacterium leprae synthesizes a unique phenolic glycolipid (PGL-I) in abundant quantities.
We studied the effect of PGL-I on the generation of superoxide anion (O-2) by stimulated human monocytes.
Peripheral blood monocytes pretreated with PGL-I released less O-2 when stimulated with M.
leprae than did control monocytes.
Monocytes pretreated with dimycocerosyl phthiocerol, mycoside A of Mycobacterium kansasii, or mycoside B of Mycobacterium microti, on the other hand, released O-2 in quantities comparable to control monocytes in response to M.
leprae stimulation.
Monocyte O-2 release in response to other stimuli of the oxidative metabolic burst, such as PMA, zymosan, Mycobacterium bovis Bacille Calmette-Guérin, or M.
kansasii, was unaffected by lipid pretreatment.
These findings demonstrate that PGL-I has a direct effect on monocyte O-2 generation in response to M.
leprae and suggest that PGL-I is a modulator of phagocytic cell function.

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