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Results for “TUBERCULOSIS IMMUNITY”

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At least 145 records · Page 8Linked to original sources
PubMed2005

DNA electroporation prime and protein boost strategy enhances humoral immunity of tuberculosis DNA vaccines in mice and non-human primates.

DNA vaccines have shown to induce strong immune response in small animals; however, its capacity of inducing robust antigen-specific immune responses in large animals is limited. In the present study, in vivo electroporation (EP) was applied and the effect of EP on humoral immune response against tuberculosis (TB) induced by DNA vaccination was tested in mice and rhesus macaques. Mice injected with 10 microg DNA encoding Ag85A and ESAT-6 followed by EP showed a reproducible humoral immunity which was equal to that obtained by using 100 microg DNA without EP. Boosting the DNA/EP treated animals with corresponding recombinant protein (50 microg of either Ag85A or ESAT-6) without adding adjuvant gave more than a 7-8-fold increase in the antibody titre but only 3-4-fold increase was found in the mice receiving 100 microg DNA without EP followed by protein boost. In concordance with the results obtained in mice, the monkeys received less DNA achieved equal high antibody responses to those induced by high dosage of DNA. Boosting the the DNA/EP treated monkeys with TB protein (500 microg of either Ag85A or ESAT-6) improved the humoral response by 7-8-fold increase in antibody titre, indicating electroporation's ability to compensate lower DNA concentration and enhance humoral immunity of TB DNA vaccines in mice and non-human primates.

Animals↗
PubMed2000

Restoration of cellular immunity against tuberculosis in patients coinfected with HIV-1 and tuberculosis with effective antiretroviral therapy: assessment by determination of CD69 expression on T cells after tuberculin stimulation.

Whether immunity against opportunistic pathogens can be fully restored by control of HIV-1 replication remains open to question. This longitudinal study was conducted to measure anti-tuberculosis (TB) cellular immunity in 13 HIV-1/TB-coinfected patients effectively treated by highly active antiretroviral therapy (HAART) in a period of 12 months. In this study, anti-TB cellular immunity was assessed by determining the frequencies of CD 69 expression on CD4+ and CD8+ T cells in response to purified protein derivative (PPD) stimulation (abbreviated as %CD4+CD69 to PPD and %CD8+CD69 to PPD). Here, we show that %CD4+CD69 to PPD correlated with the results of tuberculin skin tests and interferon-gamma (IFN-gamma) production from PPD-stimulated CD4+ T cells, and %CD8+CD69 to PPD also correlated with CD8+ T cell-mediated PPD-specific cytolysis. In overall analysis for these 13 patients, both %CD4+CD69 to PPD and %CD8+CD69 to PPD increased significantly during the 12 months (p =. 003 and p <.001, respectively). However, we found %CD4+CD69 to PPD or %CD8+CD69 to PPD failed to increase substantially in some patients (i.e., immunologic nonresponders). A significantly higher proportion of patients whose baseline CD4+ count was <50 cells/mm3 were considered to be CD4+ nonresponders compared with those whose baseline CD4+ count was >50 cells/mm3. Furthermore, baseline CD4+ cell count in nonresponders is significantly lower than that in responders, although the effectiveness of HAART did not differ between them. Our results indicate that PPD-specific frequencies of CD69 expression may be used as surrogate markers of anti-TB cellular immunity. By this method, we show that full reconstitution of anti-TB cellular immunity in HIV-1/TB coinfected patients may not necessarily be achieved by "successful" HAART and may be influenced by the baseline immune status when HAART is started. These data suggest that the decision to discontinue secondary prophylaxis for opportunistic infections should be cautiously made, even when the CD4+ cell count has significantly increased.

AIDS-Related Opportunistic Infections↗
PubMed2004

Immunity to tuberculosis.

Only 5 to 10% of immunocompetent humans are susceptible to tuberculosis, and over 85% of them develop the disease exclusively in the lungs. Human immunodeficiency virus (HIV)-infected humans, in contrast, can develop systemic disease that is more quickly lethal. This is in keeping with other evidence showing that susceptible humans generate some level of Th1 immunity to Mycobacterium tuberculosis (Mtb) infection. Tuberculosis in mice is also exclusively a lung disease that is progressive and lethal, in spite of the generation of Th1-mediated immunity. Thus mouse tuberculosis is a model of tuberculosis in susceptible humans, as is tuberculosis in guinea pigs and rabbits. Inability to resolve infection and prevent disease may not be a consequence of the generation of an inadequate number of Th1 cells but of an intrinsic deficiency in macrophage function that prevents these cells from expressing immunity. If this proves to be true, vaccinating susceptible humans against tuberculosis will be a difficult task.

Animals↗
PubMed2007

Immunological responses and protective immunity against tuberculosis conferred by vaccination of Balb/C mice with the attenuated Mycobacterium tuberculosis (phoP) SO2 strain.

The Mycobacterium tuberculosis phoP mutant strain SO2 has been shown previously to be more attenuated than Mycobacterium bovis bacillus Calmette-Guérin (BCG) and confers protective immunity against tuberculosis in mice and guinea pig models. In this study we have investigated the survival and immunological responses of Balb/c mice infected with the M. tuberculosis SO2 strain. All Balb/C mice survived intratracheal infection with M. tuberculosis SO2 strain under conditions where all the mice infected with the parental M. tuberculosis MT103 had died after 9 weeks. Infection of Balb/c mice with M. tuberculosis SO2 was associated with comparatively lower levels of interferon (IFN)-gamma, interleukin (IL)-4 and tumour necrosis factor (TNF)-alpha and higher levels of inducible nitric oxide synthase (iNOS) during the late stage of infection, when compared with M. tuberculosis MT103 infection. The delayed-type hypersensitivity (DTH) response against M. tuberculosis culture filtrates was similar in mice infected with either the M. tuberculosis phoP SO2 strain or M. tuberculosis MT103. The protective efficacy of M. tuberculosis SO2 was compared with M. bovis BCG when delivered subcutaneously to groups of Balb/C mice. Following intratracheal challenge with M. tuberculosis H37Rv, protection was generated by 60 days post-challenge in mice vaccinated with either vaccine. At day 120 post-challenge the levels of protection were still significantly greater when compared with the non-vaccinated control group. The levels of protection conferred by vaccination with M. tuberculosis SO2 or with M. bovis BCG were similar, as measured by granuloma coalescence and pneumonia in addition to growth reduction of M. tuberculosis H37Rv.

Animals↗
PubMed2006

Assessment of in vitro immunity to Mycobacterium tuberculosis in a human peripheral blood infection model using a luciferase reporter construct of M. tuberculosis H37Rv.

Protective immune responses to tuberculosis in man are primarily cell-mediated and require the interaction of specific T cells, cytokines and activated macrophages. In the present study, Mycobacterium tuberculosis H37Rv labelled with luciferase reporter enzyme was used to analyse the anti-mycobacterial immunity in man using an in vitro whole blood infection model. Peripheral blood samples obtained from M. bovis bacille Calmette-Guérin (BCG)-vaccinated tuberculin-positive healthy volunteers (n = 23) were cultured with M. tuberculosis H37Rv reporter strain. The growth of bacteria in the whole blood cultures was monitored after 48 and 96 h of infection. The results showed that the growth of M. tuberculosis was significantly inhibited after 96 h (P < 0.029) of culture. Among the cytokines studied, interleukin (IL)-10 and IL-12 were not detected at all, whereas low levels of interferon (IFN)-gamma after 96 h (0.4 IU/ml) and tumour necrosis factor (TNF)-alpha after 48 (135 pg/ml) and 96 h (47 pg/ml) of culture were detected in the supernatants of whole blood infected with M. tuberculosis. The magnitude of bacterial growth correlated directly with the concentration of TNF-alpha detected after 48 h (r = 0.722) and 96 h (r = 0.747) of culture (P <or= 0.0001 and P <or= 0.0001, respectively). However, the addition of monoclonal antibodies specific to TNF-alpha and IFN-gamma to the blood cultures did not alter mycobacterial growth indicating the role of other mechanisms/factors in restricting the growth of M. tuberculosis in whole blood cultures.

Antibodies, Monoclonal↗
PubMed1958

Airborne immunization against tuberculosis.

Inhalation of very small numbers of living attenuated (BCG) organisms and their multiplication in guinea pigs results in the development of acquired resistance against subsequent airborne infection with virulent tubercle bacilli. Different strains of BCG have differing capacities to immunize by this means.

Animals↗
PubMed1970

Demonstration in tissue culture of lymphocyte-mediated immunity to tuberculosis.

We have shown that splenic lymphocytes from mice immunized with viable attenuated mycobacterial cells (H37Ra) or ribonucleic acid prepared from these cells will bring about inhibition of multiplication of virulent tubercle bacilli (H37Rv) within normal mouse peritoneal macrophages in tissue culture. Apparently these lymphocytes, when stimulated with viable virulent tubercle bacilli, elaborate a filterable substance(s) which is responsible for this intracellular growth inhibitory effect.

Journal Article↗
PubMed2005

Strain-specific mycobacterial lipids and the stimulation of protective immunity to tuberculosis.

Control of Mycobacterium tuberculosis (M. tuberculosis) infection is dependent on recognition of bacilli by cells of the innate immune system in the lung and the subsequent generation of an acquired effector T lymphocyte response. Lipid moieties of M. tuberculosis are important stimulators of innate immunity mediated predominantly through recognition by Toll-like receptors. In this paper, we will discuss how the lipid composition of different clinical isolates (strains) of M. tuberculosis affect that strain's ability to direct innate immunity, and ultimately influence whether infection is controlled or active disease develops.

Antigen Presentation↗
PubMed1987

Aging and immunity to tuberculosis: increased susceptibility of old mice reflects a decreased capacity to generate mediator T lymphocytes.

This study employed an experimental mouse model of Mycobacterium tuberculosis infection to investigate the effects of aging on T cell-mediated protective cellular immunity. It was found that although mice of 3 to 18 mo of age were fully resistant to a standard immunizing dose of Mycobacterium tuberculosis, progressive mortality was observed in old (24 to 28 mo) mice. Death of these older animals was associated with an inability to contain or to eliminate the mycobacterial infection in the spleen and liver, and with an inability to prevent the progressive growth of the infection in the lungs. It was then revealed by the use of reciprocal passive cell transfer experiments that the age-related susceptibility of old mice reflected an inability to generate mediator protective T lymphocytes in response to the infection. In contrast, no evidence was obtained to indicate any defect at the effector cell (macrophage) level, as evidenced primarily by the finding that immune T cells from young mice conferred equivalent levels of immunity upon both old and young recipients. The results suggest therefore that T cell-mediated immunity undergoes an age-related decline in terms of its ability to respond to infection with Mycobacterium tuberculosis.

Aging↗
PubMed1995

Animal models of protective immunity in tuberculosis to evaluate candidate vaccines.

While the etiology of tuberculosis is well understood, the nature of the protective immune response to the causative mycobacteria has remained a mystery. There is an urgent need to define protective immunity critically, and to develop alternative animal models to evaluate the efficacy of new-generation vaccines against tuberculosis in a cost-effective way.

Animals↗