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M. Tuberculosis Infection (m + tuberculosis_infection)

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Medical Sciences100%

Selected Abstracts

How B cells shape the immune response against Mycobacterium tuberculosis

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 3 2009
Paul J. Maglione
Abstract Extensive work illustrating the importance of cellular immune mechanisms for protection against Mycobacterium tuberculosis has largely relegated B-cell biology to an afterthought within the tuberculosis (TB) field. However, recent studies have illustrated that B lymphocytes, through a variety of interactions with the cellular immune response, play previously underappreciated roles in shaping host defense against non-viral intracellular pathogens, including M. tuberculosis. Work in our laboratory has recently shown that, by considering these lymphocytes more broadly within their variety of interactions with cellular immunity, B cells have a significant impact on the outcome of airborne challenge with M. tuberculosis as well as the resultant inflammatory response. In this review, we advocate for a revised view of TB immunology in which roles of cellular and humoral immunity are not mutually exclusive. In the context of our current understanding of host defense against non-viral intracellular infections, we review recent data supporting a more significant role of B cells during M. tuberculosis infection than previously thought. [source]

Accelerated induction of mycobacterial antigen-specific CD8+ T cells in the Mycobacterium tuberculosis -infected lung by subcutaneous vaccination with Mycobacterium bovis bacille Calmette,Guérin

IMMUNOLOGY, Issue 4 2009
Dilara Begum
Summary Both CD4+ and CD8+ T cells are important in protection against Mycobacterium tuberculosis infection. To evaluate the effect of vaccination with Mycobacterium bovis bacille Calmette,Guérin (BCG) on the CD8+ T-cell response to pulmonary M. tuberculosis infection, we analyzed the kinetics of CD8+ T cells specific to the mycobacterial Mtb32a309,318 epitope, which is shared by M. tuberculosis and M. bovis BCG, in the lung of mice infected with M. tuberculosis. The CD8+ T cells were detected by staining lymphocytes with pentameric major histocompatibility complex (MHC) class I H-2Db,Mtb32a209,318 peptide complex and were analysed by flow cytometry. Mtb32a-specific CD8+ T cells became detectable on day 14, and reached a plateau on day 21, in the lung of M. tuberculosis -infected unvaccinated mice. Subcutaneous vaccination with M. bovis BCG in the footpads induced Mtb32a-specific CD8+ T cells in the draining lymph nodes (LNs) on day 7 and their numbers further increased on day 14. When M. bovis BCG-vaccinated mice were exposed to pulmonaryinfection with M. tuberculosis 4 weeks after vaccination, the Mtb32a-specific CD8+ T cells in the infected lung became detectable on day 7 and reached a plateau on day 14, which was 1 week earlier than in the unvaccinated mice. The pulmonary CD8+ T cells from the BCG-vaccinated M. tuberculosis -infected mice produced interferon-, in response to Mtb32a209,318 peptide on day 7 of the infection, whereas those of unvaccinated mice did not. The results demonstrate that induction of mycobacterial antigen-specific protective CD8+ T cells in the M. tuberculosis -infected lung is accelerated by subcutaneous vaccination with M. bovis BCG. [source]

4254: Infectious and non infectious triggers in non-infectious uveitis

ACTA OPHTHALMOLOGICA, Issue 2010
G WILDNER
Purpose The induction of autoimmune uveitis is difficult to explain with respect to the immune privileged status of the eye. The intact BRB can only be passed by already activated leukocytes, which should normally be ignorant to the sequestered intraocular antigens. Antigenic mimicry of retinal autoantigens by environmental proteins could explain extraocular activation of effector T cells. Methods We have previously demonstrated antigenic mimicry of a peptide from retinal S-Antigen and peptides from rotavirus (Rota) and bovine milk casein (Cas). Both, Rota and Cas, induce T cell lines cross-reactive with retinal S-Ag peptide as well as experimental autoimmune uveitis in rats. Patients with uveitis have increased antibody and T cell responses to the mimicry peptides as well as to the S-Ag peptide compared to healthy donors. Accordingly, Infection with rotavirus or any gastrointestinal pathogen with concomitant ingestion of bovine milk products could induce an immune response in the gastrointestinal tract that is cross-reactive with ocular autoantigens and lead to induction of autoimmunity in the eye. Results Uveitis as a well known adverse effect after BCG (Bacille Calmette Guerin) treatment might also be the result of antigenic mimicry. We have shown T cell responses to PPD from M. tuberculosis and the retinal autoantigens S-Ag, IRBP and CRALBP from a patient who had developed granulomatous uveitis after BCG application for bladder carcinoma. Data base searches revealed a number of amino acid sequence homologies between proteins from mycobacteria and retinal autoantigens, suggesting antigenic mimicry. These findings might as well be an explanation for the occurrence of uveitis in connection with M. tuberculosis infection, even when no mycobacteria are detectable in the eye. [source]

Comparative Evaluation of Cytokines, T-Cell Apoptosis, and Costimulatory Molecule Expression in Tuberculous and Nontuberculous Pleurisy

CLINICAL AND TRANSLATIONAL SCIENCE, Issue 3 2008
Priya Rajavelu M.Sc.
Abstract In this study, we compared several immune parameters in tuberculosis (TB) and nontuberculosis (NTB) pleurisy to gain an understanding of the mechanism behind enhanced Th1 apoptosis that occurs at sites of active Myobacterium tuberculosis (M. tuberculosis) infection. An initial evaluation of the accumulated cytokines in pleural fluid (PF) demonstrated that both TB and NTB pleurisy were associated with prointflammatory cytokines, while only TB pleurisy had augmented expression of interferon (IFN)-, and soluble Fas ligand (sFASL). Despite enhanced expression of the apoptosis-inducing molecule in TB pleurisy, T cells derived from both types of pleurisy exhibited significant apoptosis. In both groups, T-cell apoptosis correlated with low expression of CD80 on PF-derived macrophages and elevated accumulation of TGF-, in the PF. A causative correlation between TGF-, and low CD80 expression in the two groups was established by in vitro studies demonstrating TGF-, inhibition of CD80 upregulation in a macrophage cell line. Together, the findings allude to the possibility that activation in the absence of appropriate CD80 costimulation is the mechanism that leads to T-cell apoptosis at sites of active M. tuberculosis infection. Furthermore, the findings also indicate that T-cell apoptosis is perhaps a host regulatory mechanism to limit inflammation, rather than a pathogen-induced immune deviation. [source]

Mycobacterial infection in a series of 1261 renal transplant recipients

CLINICAL MICROBIOLOGY AND INFECTION, Issue 6 2003
J. A. Queipo
Objective To describe the incidence and clinical characteristics of mycobacterial infection in renal transplant recipients. Methods We retrospectively analyzed the cases of mycobacterial infection in a series of 1261 renal transplants carried out in our Unit of Renal Transplantation from 1980 to 2000. Demographic parameters and clinical antecedents such as age, cause of end-stage renal disease, time of follow-up of the graft, previous renal function and type of immunosuppression were considered. Moreover, the clinical onset, diagnostic tools, treatment policy and evolution were studied. The pathogenesis of the different types of mycobacteria isolated was also analyzed. Diagnosis was made with the Ziehl,Neelsen staining method. Culture was performed by the conventional Löwenstein,Jensen method and the Bactec-460 radiometric method. Results We found mycobacterial infection in 27 patients (2.1%), due to Mycobacterium tuberculosis in 20 cases, M. kansasii in five patients, and M. fortuitum in two patients. The mean elapsed time from the renal transplant was 20.5 months; the infection appeared in 18 patients during the first eight months after transplantation. The clinical onset was pulmonary infection in 17 cases (12 M. tuberculosis and five M. kansasii); five had urinary symptoms (three M. tuberculosis and two M. fortuitum); three cases of M. tuberculosis infection had abdominal symptoms; another one began with a perineal tuberculous abscess; the rest of the patients were asymptomatic. The types of specimen on which microbiological identification was carried out were, in decreasing order: sputum and/or bronchial washing/pleural aspiration, urine, feces, gastric and peritoneal fluids, bone marrow and blood. The first-line drug isoniazid had the highest resistance index in the susceptibility test. Clinical dissemination was observed in eight patients, four of whom died. Another three patients had a significant impairment in renal function, and in one of these patients an allograft nephrectomy was necessary due to a severe septic syndrome. Conclusions Mycobacterial infection, mainly by M. tuberculosis, has an important impact on kidney transplant recipients, particularly during the first year after surgery. Diagnosis often presents some difficulties, and a delay in treatment represents a determinant factor for the evolution, with a risk of death or permanent damage in renal function. Therefore, early diagnosis is mandatory. When the Mantoux reaction is positive, antituberculous prophylaxis seems advisable. [source]