| The effects of mycobacterium tuberculosis on alveolar macrophages. |
|
Keon Youl Kim, Kye Young Lee, In Kyu Hyun, Young Whan Kim, Sung Koo Han, Young Soo Shim, Yong Chol Han |
|
Department of Internal Medicine & Tuberculosis Research Institute, Seoul National University College of Medicine, Seoul, Korea |
|
|
| Abstract |
Background
The oxygen radicals released by alveolar macrophages contribute to killing of microorganisms including M. tuberculosis. Macrophages are “ primrd" for enhanced oxygen radical release by macrophage activator like IFN -γ and LPS, which do not themselves cause release of oxygen radicals. Actural production of oxygen radicals is “ triggered" by phagocytosis or by exposure to chemical stimuli like PMA or FMLP. There has been debates about the priming effect of alveolar macrophages because they are exposed to usual environmental particles unlike blood monocytes.
Therefore we examined priming effect of IFN - γ in human alveolar macrophages comparing with that in blood monocytes and rat alveolar macrophages. And we observed the alterations of superoxide production in both human and rat alveolar macrophages after exposure to M . tuberculosis H37Ra bacilli itself and its lysate.
Methods
Bronchoalveolar lavage fluid was processed to isolate alveolar macrophages by adherence and the adherent cells were removed by cold shock method. After exposure to M. tuberculosis H37Ra strain, alveolar macrophages were incubated for 24 hours with IFN-γ The amount of superoxide production stimulated with PMA was measured by ferricytochrome C reduction method.
Results
1) The priming effect in human alveolar macrophages was not obseπed even with high concentration of IFN-γ while it was observed in blood monocytes and rat alveolar macrophages.
2) Both human and rat alveolar macrophages exposed to avirulent H37Ra strain showed triggering of superoxide release and similar results were shown with the exposure to H37Ra lysate.
Conclusions
The priming effect in human alveolar macrophages is not observed because of its usual exposure to environmental particles and avirulent H37Ra strain does not inhibit the activation of alveolar macrophages. |
| Key Words:
Tuberculosis, H37Ra, Macrophage, IFN-γ, Priming |
|
PDF Links
Full text via DOI
Download Citation
