Mycobacterium tuberculosis is capable of intracellular growth inside the phagosomes of monocytes and macrophages. Therefore, M. tuberculosis produce progressive disease relying on both its virulence and the inherent microbicidal ability of the
monoctyte
that ingests it, At present no single structure of the organism can explain its virulence. But complex lipophilic macromolcules which M. tuberculosis abundantly contains confer properties that enable the organism to resist adverse environmental
conditions, and among them some have been associated with the virulence of the organism.
Recently a phenolic glycolipid, PGL-Tb, unique to M. tuberculosis was isolated and characterized. Considering the role of a phenolic glycolipid of M. leprae in leprosy, PGL-Tb may play a specific role in the pathogenesis of tuberculosis. In this
study,
therefore, the effect of PGL-Tb on the proliferation of the organisms within monocytes was examined, and the PGL-Tb content of clinical isolates was compared with clinical type of tuberculosis patients.
@ES The results were as follows.
@EN 1. Among the C1 siolate, strain Erdman and strain Canetti, the C1 isolate(PGL-Tb content : <0.1μg/mg dry weight of bacilli) showed the shortest intracellular mean eneration time in human monocytes. And intracerllular mcan generation time of
strain
Erdman(PGL-Tb content : 0.1μg/mg dry weight of bacilli) was shorter than that of strain Canetti(PGL-Tb content : 0.5μg/mg dry weight of bacilli).
2. The PGL-Tb content of 32 M. tugerculosis clinical isolates measured by a competitive ELISA ranged from than 0.1μg/ml dry weight of bacilli to 1.83μg/mg dry weight of bacilli.
3. Mean PGL-Tb content of clinical isolates from tuberculosis patients of minimal advanced type was 0.72±0.58%μg, that from those of moderate advanced type was 0.73±0.58μg, and that from those of far advanced type was 0.44±0.24㎍.
Thus there was no significant relationship of PGL-Tb content in M. tuberculosis strains to generation time of the organism in monocyte and to clinical type of tuberculosis patients. These results suggest that PGL-Tb may not be involved directly
pathogenesis of tuberculosis.
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