Chronic infection due to mycobacterium intracellulare in mice: association with macrophage release of prostaglandin E/sub 2/ and reversal by injection of indomethacin, muramyl dipeptide, or interferon-. gamma
As a model for the study of human atypical mycobacterial disease, the basis for the prolonged mycobacteriosis in mice infected with Mycobacterium intracellulare was studied. Two weeks after i.v. injection of mycobacteria, peritoneal macrophages were found to be activated, as indicated by their capacity to produce large amounts of superoxide anion (O/sub 2//sup -/) in response in phorbol myristate acetate (PMA) or viable M. intracellulare. However, 4 wk after infection, despite the continued presence of large numbers of mycobacteria in the spleen, macrophages from infected animals produced low amounts of O/sub 2//sup -/. Additional investigation showed that macrophages from infected animals produced large amounts of prostaglandin E/sub 2/ (PGE/sub 2/) when stimulated by mycobacterial antigens. In vitro, such concentrations of PGE/sub 2/ inhibited uptake of (/sup 3/H)thymidine by stimulated spleen lymphocytes from infected animals. The results support the concept that interaction between the host and M. intracellulare is modulated profoundly by PG and suggest that administration of agents that directly promote macrophage activation can enhance resistance to infection by this organism.
- Research Organization:
- National Jewish Center for Immunology and Respiratory Medicine, Denver, CO
- OSTI ID:
- 6935919
- Journal Information:
- J. Immunol.; (United States), Vol. 136:5
- Country of Publication:
- United States
- Language:
- English
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