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Biomedical subjects

M J Lefford

Publications and source records attributed to M J Lefford.

47 records · Page 3Linked to original sources
PubMed1973

Immune response to Mycobacterium tuberculosis in rats.

After intravenous injection into rats, both the attenuated strain R1Rv and the virulent strain H37Rv of Mycobacterium tuberculosis grow in the liver and spleen. However, the infected rats mount a specific immune response with great rapidity, giving a false impression of natural resistance to the tubercle bacillus. Adoptive immunity to tuberculosis was achieved by transferring thoracic duct cells from immunized donors to normal syngeneic recipients. The transferred immunity was vested in a population of lymphocytes uncontaminated with macrophages. The adoptive immunity was effectively expressed against both attenuated and virulent tubercle bacilli, and it was shown to be immunologically specific. Lymphocytes which conferred immunity to tuberculosis were not protective against Listeria monocytogenes infection, and vice versa. Immunity could not be transferred with either normal thoracic duct lymphocytes (TDL), heat-killed sensitized TDL, or serum from specifically immunized donors. The ability of TDL from BCG-immunized donors to confer immunity was maintained at an unimpaired level for at least 3 months after immunization.

Animals↗
PubMed1969

The host response to Calmette-Guérin bacillus infection in mice.

Heterologous organisms (L. monocytogenes and S. typhimurium) were used to study the rate of development, magnitude, and persistence of the antimicrobial resistance engendered in mice by vaccination with BCG. These same methods were used to investigate the influence of prior vaccination on the host response to reinfection. The rate of onset and magnitude of the resistance produced by BCG varied with the vaccinating dose. Increased resistance was detected within 48 hr of injecting large numbers of BCG (approximately 10(8) viable units), but concurrent treatment with isoniazid interrupted its further development. An equal number of heat-killed organisms failed to influence host resistance significantly. The development of tuberculin sensitivity was also dependent upon the continued survival of the immunizing population of BCG. When vaccinated mice were reinfected with BCG, host resistance in spleen and liver was rapidly augmented to the accompaniment of striking changes in the morphology and microbicidal activity of the peritoneal macrophages. These changes occurred most rapidly in mice with a high level of delayed hypersensitivity at the time of reinfection.

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