Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells

Experiments were performed to determine the effects of Mycobacterium tuberculosis-derived sulfolipid I on phagocytic cells. Sulfolipid I was taken up in significant amounts by human neutrophils and in lesser amounts by monocytes and lymphocytes. Superoxide (O2-) production by neutrophils was significantly increased by sulfolipid I, but the rate of production was slower than that reported previously for other stimuli. The optimal concentration of sulfolipid I for stimulation of O2- production was 27 micrograms/ml, while higher concentrations produced less. At substimulatory levels sulfolipid I caused enhancement of O2- release from neutrophils when it was subsequently stimulated by other agents. Nonadherent monocytes from most normal donors failed to produce O2- when treated with sulfolipid I; however, adherent monocytes pretreated with gamma interferon did produce O2- with sulfolipid I stimulation. Priming for an enhanced oxidative response of activated monocytes was also observed. These sulfolipid I-induced changes in phagocytic cell function may be important in altering the ability of phagocytes to respond effectively to M. tuberculosis and may also cause exaggerated inflammatory responses.