Immunomodulation of mouse macrophage killing of Mycobacterium avium in vitro.
When C57BL/6 mice were infected intravenously with Mycobacterium avium, bacterial growth continued within the spleen until more than 10(8) CFU/g of tissue were attained. This contrasted with Mycobacterium bovis BCG infections where growth declined after 2 weeks. In vivo M. avium-infected splenic macrophages were harvested from chronically infected mice and cultured in vitro for 4 days at 37 degrees C. The number of viable mycobacteria within the resulting macrophage monolayers decreased when cultured in the presence of autologous sensitized T cells and an exogenous source of interleukin-2 (recombinant interleukin-2; 50 U/ml) compared with untreated controls (P less than 0.05). Incubation of the infected macrophages with autologous T cells and soluble M. avium antigens also significantly reduced the number of viable organisms. These results indicate that the mycobactericidal activity of M. avium-infected macrophages can be enhanced in a way that may have important therapeutic implications for patients infected with this opportunistic pathogen.
Hubbard
R D
RD
Trudeau Institute, Inc., Saranac Lake, New York 12983.
Collins
F M
FM
D000818:Animals; D003602:Cytotoxicity, Immunologic; D007371:Interferon-gamma / Q000096:biosynthesis; D008264:Macrophages / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009162:Mycobacterium avium / Q000254:growth & development / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology; D014376:Tuberculosis / Q000628:therapy; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma