![]() ![]() Several members of the genus Mycobacterium (i.e. The initial contact between the mycobacteria and the phagocytic cell is in all probability of great importance for the phagocytic process and it is likely that mycobacterial surface molecules, such as the complex cell wall glycolipids, are of importance for the outcome of such an interaction. Little is known, however, about the molecular mechanisms responsible for the mycobacterial resistance to destruction by the phagocytes. Pathogenic mycobacteria have the capacity to survive and multiply inside phagocytic cells. The subcellular localization of the reactive oxygen metabolites formed was related to the way in which the glycolipids were presented to the cells. The complement receptor 3 (CR3) has earlier been shown to be of importance for the phagocyte binding of mycobacteria, but did not appear to be involved in the activation of neutrophils by PGLs. kansasii contain tri- and tetrasaccharides, respectively, while the nonactivating PGLs from M. This is in line with the fact that the activating PGLs from M. The activation, however, could not be inhibited by rhamnose or fucose, indicating a complex interaction which probably involves more than one saccharide unit. tuberculosis PGL decreased the production of oxygen radicals, showing the importance of the PGL carbohydrate moiety for the interaction. The PGLs from Mycobacterium tuberculosis and Mycobacterium kansasii, respectively, were shown to stimulate the production of oxygen metabolites, while PGLs from Mycobacterium marinum and Mycobacterium bovis BCG, respectively, were unable to induce an oxidative response. Human neutrophils were allowed to interact with each of four purified mycobacterial PGLs and the neutrophil production of reactive oxygen metabolites was followed kinetically by luminol-/isoluminol-amplified chemiluminescence. The interaction between mycobacterial phenolic glycolipids (PGLs) and phagocytes was studied.
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