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pubmed:abstractText |
We examined the capacity of human neutrophils to develop a respiratory burst, as monitored by superoxide release, in response to interaction with Mycobacterium tuberculosis. Serum-opsonized, heat-killed mycobacteria induced significant release of superoxide from neutrophils after 30 min of exposure, with a maximum release of 34 +/- 1.7 nmol/30 min per 5 X 10(6) neutrophils occurring with a mycobacterium/neutrophil ratio of 40:1. Similar levels of superoxide release were induced by live mycobacteria. Neutrophil superoxide production was reduced significantly with exposure to unopsonized organisms or by substitution of heat-inactivated serum for opsonization. Mycobacterial components including culture filtrate, purified protein derivative, and the cell wall polysaccharide arabinogalactan failed to induce significant release of superoxide from neutrophils. Transmission electron microscopy demonstrated that more than 90% of the neutrophils had ingested heat-killed mycobacteria concomitant with the development of respiratory burst activity. These data suggest that the presumed failure of neutrophil killing of mycobacteria cannot be attributed to a lack of phagocytosis or respiratory burst activation.
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