This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Takashima, T Articles by Collins, F M Search for Related Content PubMed PubMed Citation Articles by Takashima, T Articles by Collins, F M

 Previous Article  |  Next Article 

Infect Immun. 1988 November; 56(11): 2782-2787

T-cell-mediated immunity in persistent Mycobacterium intracellulare infections in mice.

Trudeau Institute, Inc., Saranac Lake, New York 12983.

ABSTRACT

Growth of mouse-virulent Mycobacterium intracellulare D673 and TMC 1405 in the lung was affected by T-cell depletion in susceptible C57BL/6 mice. Significant differences also occurred between the growth patterns seen in congenitally athymic (nu/nu) mice and their nu/+ littermates. Treatment of the mice with an immunosuppressive regimen of cyclosporin A (75 mg/kg of body weight per day subcutaneously) provided further evidence of the importance of T cells in controlling growth of M. intracellulare in the normal host. Adoptive transfer experiments indicated the presence of a T-cell-mediated specific protective immunity against a subsequent M. intracellulare challenge when transfer was carried out 3 weeks after immunization of the donor host. At this time, cross-protective immunity was also observed against a virulent M. tuberculosis challenge. There was no difference in the rate of growth by M. intracellulare as challenge in Mycobacterium bovis BCG-activated or normal peritoneal macrophages from C57BL/6 mice tested in vitro during a 7-day period. However, M. tuberculosis growth rates were decreased substantially in the BCG-activated macrophages. These studies suggest that mice infected with M. intracellulare do not eliminate the infection, because this organism can resist the bactericidal activity of the T-cell-activated macrophage better than M. tuberculosis can.