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PubMed2002

Murine Model of Tuberculosis. In vitro and in vivo Study.

Animal models that mimic the whole spectrum of susceptibility and resistance of human populations to tuberculosis would be useful for studying pathogenesis of tuberculosis, mechanisms of the host defense, and for testing prospective prophylactic and therapeutic tuberculosis vaccines and drugs. Inbred mouse strains are broadly and successfully used to model human tuberculosis and study mechanisms of host-mycobacteria interaction. Here we consider numerous aspects of murine models of tuberculosis. We analyze the course of tuberculosis depending on route and dosage of mycobacterial infection, and discuss the conformity of these approaches to the natural route of human infection. The advantage of the mouse model is provided by the availability of hundreds of inbred strains with different genetic background. It allows a genetic analysis of the mouse susceptibility/resistance to tuberculosis. Mouse strains with specific properties such as congenic, recombinant, recombinant inbred, recombinant congenic, mutant and usage of whole genome screening led to mapping loci controlling these traits. Transgenic mouse strains with gene insertion or targeted mutation (knock-out of a gene) are very effective tools for studying the role of specific genes controlling the anti-tuberculosis immunity. Mice with knock-out genes for cytokines, chemokines, cell subpopulations, cell receptors, and enzymes are broadly used to identify the mechanisms of tuberculosis control. In this review we examine a mouse model for anti-tuberculosis vaccine and drug testing. In addition, we present some important phenomena of tuberculosis immunity - latent tuberculosis/reactivation and immunological memory to tuberculosis.

Animals↗
PubMed1996

[Commemorative lecture of receiving Imamura Memorial Prize. Analysis of cellular immunity against tuberculosis in man with special reference to tuberculous pleurisy and cytokines].

Because of containing of numerous immunocompetent cells, tuberculous pleurisy is a good model for analysis of local cellular immunity. When lymphocytes in pleural effusion were cocultured with purified protein derivative (PPD), they reacted to PPD and produced far more interleukin 2 (IL-2) and interferon-gamma (IFN-gamma) than did peripheral blood lymphocytes. Analysis using monoclonal antibody and complement revealed that at least the OKT4+/OKT8- T-cell subset is responsible for the antigen-specific IFN-gamma production in pleural fluid T lymphocytes. Tuberculous pleural fluid itself had far higher levels of IL-2 and IFN-gamma than malignant pleural fluid. Therefore, it is indicated that activated T lymphocytes in tuberculous pleural fluid concern the production of lymphokines at the morbid site. Treatment with IFN-gamma resulted in an increased percentage of human alveolar macrophages ingesting BCG and an increased number of ingested BCG in individual alveolar macrophage in patient with pulmonary tuberculosis. The IFN-gamma treatment also showed increased killing activity of alveolar macrophages. Through these studies, IFN-gamma is an essential cytokine which activates human alveolar macrophages and induces antimycobacterial activity. In conclusion, we could elucidate from the study of tuberculous pleurisy that exudative sensitized pleural fluid T-lymphocytes play a major role in the defence of tuberculosis at the morbid site.

Humans↗
PubMed1995

[Some problems concerning local cellular immunity in tuberculosis].

Tuberculous pleurisy is restricted to the pleural cavity and profuse pleural fluid, which contains numerous immunocompetent cells, is easily obtained. Therefore, tuberculous pleurisy is a good model for the study of local cellular immunity. The characteristics and function of lymphocytes in both pleural exudate and peripheral blood were studied. The pleural fluid had more T-lymphocytes than the peripheral blood. To evaluate predominant T-lymphocyte function in tuberculous pleural exudate, we studied the reactions of the lymphocytes to the specific antigen. When lymphocytes in pleural effusion were cocultured with purified protein derivative (PPD), they reacted to PPD and produced far more interferon-gamma (IFN-gamma) than did peripheral blood lymphocytes. Thus, exudative-sensitized lymphocytes in morbid sites reacted to the specific antigen more strongly. These observations indicate the presence of local cellular immunity in tuberculous pleurisy at the morbid site. It would be very interesting to know which T-cell subset produces IFN-gamma. When pleural fluid T lymphocytes were treated with OKT4 monoclonal antibody and complement, a significant decrease in IFN-gamma production was observed in all patients examined, whereas no definite decrease in IFN-gamma production was found after treatment with OKT8 monoclonal antibody and complement. These results suggest that at least the OKT4+/OKT8- T-cell subset is responsible for the antigen-specific IFN-gamma production in pleural fluid T lymphocytes. With the cooperation of macrophages or monocytes, pleural fluid T lymphocytes produced a significant level of interleukin 2 (IL-2) in the presence of PPD. Tuberculosis pleural fluid macrophages promoted greater IL-2 production than blood monocytes from either tuberculosis pleural fluid or blood T lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗