Induction of enhanced resistance against encephalomyocarditis virus infection of mice by nonviable Mycobacterium tuberculosis: mechanisms of protection.
Nonviable Mycobacterium tuberculosis strain Jamaica suspended in oil-droplet emulsions was used to enhance resistance of mice against encephalomyocarditis virus (EMCV). The mycobacteria-injected mice were significantly resistant to 50,000 50% lethal doses of EMCV. Similar concentrations of virus in plasma of normal and mycobacteria-injected mice from 1 to 120 min after injection of EMCV showed that resistance was not a result of rapid elimination of virus from the circulation. Furthermore, survival of viremic mice indicated protective mechanisms were operative after EMCV had escaped primary surveillance. Resistance did not appear to be associated with the mouse major histocompatibility gene complex. The spleen was intimately associated with protection, and the thymus was nonessential for enhanced resistance to EMCV. Protection was significantly diminished by cyclophosphamide injected intraperitoneally from 3 days before to the day of virus challenge. Finally, silica given intraperitoneally 24 h before virus completely abrogated resistance of mycobacteria-injected mice to EMCV. These results suggest that macrophages functioning independently of T-lymphocytes are important effector cells in resistance to EMCV of mice injected with nonviable mycobacteria.
D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D004686:Encephalomyocarditis virus / Q000254:growth & development; D004769:Enterovirus Infections / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D008285:Major Histocompatibility Complex; D051379:Mice; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D012822:Silicon Dioxide / Q000494:pharmacology; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D012822:Silicon Dioxide; D003520:Cyclophosphamide