Effect of Mycobacterium tuberculosis-derived sulfolipid I on human phagocytic cells
| Autor: | Burton R. Andersen, T. J. Holzer, M. B. Goren, Liang Zhang |
|---|---|
| Rok vydání: | 1988 |
| Předmět: |
Sulfolipid
Phagocyte Cell Survival Neutrophils Virulence Factors Immunology Stimulation Biology Microbiology Monocytes Interferon-gamma chemistry.chemical_compound Superoxides medicine Interferon gamma Phagocytic Cell Phagocytes Cord factor Superoxide Macrophages Monocyte Mycobacterium tuberculosis Macrophage Activation Infectious Diseases medicine.anatomical_structure chemistry Cord Factors Tetradecanoylphorbol Acetate Parasitology Glycolipids Research Article medicine.drug |
| Zdroj: | Infection and Immunity. 56:2876-2883 |
| ISSN: | 1098-5522 0019-9567 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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