Journal articles: 'M. tuberculosis Infection'

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Small, P. M. "M tuberculosis and HIV infection." Biomedicine & Pharmacotherapy 47, no. 8 (January 1993): 355. http://dx.doi.org/10.1016/0753-3322(93)90091-x.

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Reuter, Morgan A., Nicole D. Pecora, Clifford V. Harding, David H. Canaday, and David McDonald. "Mycobacterium tuberculosis Promotes HIV trans-Infection and Suppresses Major Histocompatibility Complex Class II Antigen Processing by Dendritic Cells." Journal of Virology 84, no. 17 (June 30, 2010): 8549–60. http://dx.doi.org/10.1128/jvi.02303-09.

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ABSTRACT Mycobacterium tuberculosis is a leading killer of HIV-infected individuals worldwide, particularly in sub-Saharan Africa, where it is responsible for up to 50% of HIV-related deaths. Infection by HIV predisposes individuals to M. tuberculosis infection, and coinfection accelerates the progression of both diseases. In contrast to most other opportunistic infections associated with HIV, an increased risk of M. tuberculosis infection occurs during early-stage HIV disease, long before CD4 T cell counts fall below critical levels. We hypothesized that M. tuberculosis infection contributes to HIV pathogenesis by interfering with dendritic cell (DC)-mediated immune control. DCs carry pathogens like M. tuberculosis and HIV from sites of infection into lymphoid tissues, where they process and present antigenic peptides to CD4 T cells. Paradoxically, DCs can also deliver infectious HIV to T cells without first becoming infected, a process known as trans-infection. Lipopolysaccharide (LPS)-activated DCs sequester HIV in pocketlike membrane invaginations that remain open to the cell surface, and individual virions are delivered from the pocket into T cells at the site of contact during trans-infection. Here we report that M. tuberculosis exposure increases HIV trans-infection and induces viral sequestration within surface-accessible compartments identical to those seen in LPS-stimulated DCs. At the same time, M. tuberculosis dramatically decreases the degradative processing and major histocompatibility complex class II (MHC-II) presentation of HIV antigens to CD4 T cells. Our data suggest that M. tuberculosis infection promotes a shift in the dynamic balance between antigen processing and intact virion presentation, favoring DC-mediated amplification of HIV infections.

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Naughton, James F., Katrina L. Mealey, K. Jane Wardrop, J. Lindsay Oaks, and Daniel S. Bradway. "Systemic Mycobacterium avium Infection in a Dog Diagnosed by Polymerase Chain Reaction Analysis of Buffy Coat." Journal of the American Animal Hospital Association 41, no. 2 (March 1, 2005): 128–32. http://dx.doi.org/10.5326/0410128.

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Dogs may be infected by Mycobacterium (M.) tuberculosis, M. bovis, and M. avium complex, and the clinical signs associated with each of these infections may be indistinguishable. Rapid speciation of the infecting organism is desirable because of the public health concerns associated with M. bovis and M. tuberculosis infections. A mycobacterial infection was suspected in the dog of this report based on acid-fast staining of organisms in macrophages obtained from liver aspirates and buffy-coat preparations. Polymerase chain reaction (PCR) analysis of a buffy-coat preparation identified M. avium.

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Petrenko, V. I., S. B. Noreiko, Ya V. Bondarenko, I. O. Galan, and O. V. Stopolyanskyi. "A modern view on the mechanism of occurrence and development of latent tuberculosis infection. Literature review." Tuberculosis, Lung Diseases, HIV Infection, no. 3 (September 27, 2022): 60–67. http://dx.doi.org/10.30978/tb2022-3-60.

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Сonsider the modern concept of understanding of latent tuberculosis infection. To conduct this review, 64 literature sources were analyzed using electronic databases of medical publications, mainly PubMed.About a quarter of the world's population is infected with M. tuberculosis. Most of those infected are able to contain M. tuberculosis, that is, they are in a state of latent tuberculosis infection without any manifestations of active disease. At the present stage, it is impossible to detect persistent (latent) M. tuberculosis, which makes it impossible to identify those individuals who among likely infected and asymptomatic hosts cleared of M. tuberculosis, and those who remain latently infected or latent infected will progress to failure to control M. tuberculosis and eventually develop tuberculosis. The dogma of the binary nature of M. tuberculosis infection (active tuberculosis or latent tuberculosis infection) is an oversimplified and now outdated concept. Understanding all the immune components and responses that are the essence of latent tuberculosis infection or resistance to it, to the constant control of M. tuberculosis or even their elimination from the host is crucial for understanding protective immunity from M. tuberculosis.Studies of the immune response to M. tuberculosis in people resistant to latent tuberculosis infection may provide insight into alternative mechanisms of protection against M. tuberculosis, treatment of tuberculosis, and approaches to vaccine development.

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RAIMUNDO, SILVIA MARTORANO, HYUN MO YANG, RODNEY CARLOS BASSANEZI, and MARIZETE A. C. FERREIRA. "THE ATTRACTING BASINS AND THE ASSESSMENT OF THE TRANSMISSION COEFFICIENTS FOR HIV AND M. TUBERCULOSIS INFECTIONS AMONG WOMEN INMATES." Journal of Biological Systems 10, no. 01 (March 2002): 61–83. http://dx.doi.org/10.1142/s0218339002000457.

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It has been observed that in many cases one infection can partially protect against another infection or it may lead to a co-infection. For instance, the interaction between infections with different strains, like dengue and malaria or tuberculosis and lepra, induces cross immunity. On the other hand, individuals infected with HIV are much more susceptible to other infections, for instance, tuberculosis. We propose a compartmental model to describe the transmission of AIDS and tuberculosis in a closed community as an example of one infection activating the other one. When studying the dynamics of the interactions we obtain basins of attraction where one infection prevails over the other one and where both infections coalesce. Furthermore, we are taking into account an adaptation of the model in order to assess the transmission coefficients for HIV and Mycobacterium tuberculosis infections among women inmates.

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Fontán, Patricia, Virginie Aris, Saleena Ghanny, Patricia Soteropoulos, and Issar Smith. "Global Transcriptional Profile of Mycobacterium tuberculosis during THP-1 Human Macrophage Infection." Infection and Immunity 76, no. 2 (December 10, 2007): 717–25. http://dx.doi.org/10.1128/iai.00974-07.

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ABSTRACT During lung infection, Mycobacterium tuberculosis resides in macrophages and subverts the bactericidal mechanisms of these professional phagocytes. Comprehension of this host-pathogen relationship is fundamental for the development of new therapies to cure and prevent tuberculosis. In this work, we analyzed the transcriptional profile of M. tuberculosis infecting human macrophage-like THP-1 cells in order to identify putative bacterial pathogenic factors that can be relevant for the intracellular survival of M. tuberculosis. We compared the gene expression profile of M. tuberculosis H37Rv after 4 h and 24 h of infection of human macrophage-like THP-1 cells with the gene expression profile of the strain growing exponentially in broth cultures. We found 585 genes expressed differentially by intracellular M. tuberculosis. An analysis of the gene expression profile of M. tuberculosis inside THP-1 cells suggests the perturbation of the cell envelope as a major intracellular stress inside THP-1 macrophages.

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Cheung, Chen-Yi, Matthew B. McNeil, and Gregory M. Cook. "Utilization of CRISPR interference to investigate the contribution of genes to pathogenesis in a macrophage model of Mycobacterium tuberculosis infection." Journal of Antimicrobial Chemotherapy 77, no. 3 (November 28, 2021): 615–19. http://dx.doi.org/10.1093/jac/dkab437.

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Abstract Objectives There is an urgent need for novel drugs that target unique cellular pathways to combat infections caused by Mycobacterium tuberculosis. CRISPR interference (CRISPRi)-mediated transcriptional repression has recently been developed for use in mycobacteria as a genetic tool for identifying and validating essential genes as novel drug targets. Whilst CRISPRi has been applied to extracellular bacteria, no studies to date have determined whether CRISPRi can be used in M. tuberculosis infection models. Methods Using the human monocytic macrophage-like THP-1 cell line as a model for M. tuberculosis infection we investigated if CRISPRi can be activated within intracellular M. tuberculosis. Results The transcriptional repression of two candidate M. tuberculosis genes, i.e. mmpL3 and qcrB, leads to a reduction in viable M. tuberculosis within infected THP-1 cells. The reduction in viable colonies is dependent on both the level of CRISPRi-mediated repression and the duration of repression. Conclusions These results highlight the utility of CRISPRi in exploring mycobacterial gene function and essentiality under a variety of conditions pertinent to host infection.

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Rivas-Santiago, Bruno, Stephan K. Schwander, Carmen Sarabia, Gill Diamond, Marcia E. Klein-Patel, Rogelio Hernandez-Pando, Jerrold J. Ellner, and Eduardo Sada. "Human β-Defensin 2 Is Expressed and Associated with Mycobacterium tuberculosis during Infection of Human Alveolar Epithelial Cells." Infection and Immunity 73, no. 8 (August 2005): 4505–11. http://dx.doi.org/10.1128/iai.73.8.4505-4511.2005.

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ABSTRACT To determine the role of human β-defensin 2 (HBD-2) in human tuberculosis, we studied the in vitro induction of HBD-2 gene expression by Mycobacterium tuberculosis H37Rv infection in the human lung epithelial cell line A549, in alveolar macrophages (AM), and in blood monocytes (MN) by reverse transcription-PCR. We also studied the induction of HBD-2 gene expression by mannose lipoarabinomannan (manLAM) from M. tuberculosis. Intracellular production of HBD-2 peptide was detected by immunocytochemistry and electron microscopy. Our results demonstrated that there was induction of HBD-2 mRNA in A549 cells after infection with M. tuberculosis at various multiplicities of infection (MOI) and that there was stimulation with manLAM. AM expressed the HBD-2 gene only at a high MOI with M. tuberculosis. MN did not express HBD-2 at any of the experimental M. tuberculosis MOI. Immunostaining revealed the presence of intracellular HBD-2 peptide in A549 cells following infection with M. tuberculosis, and the staining was more intense in areas where there were M. tuberculosis clusters. By using electron microscopy we also demonstrated production of HBD-2 after M. tuberculosis infection and adherence of HBD-2 to the membranes of M. tuberculosis. Alveolar epithelial cells are among the first cells to encounter M. tuberculosis following aerogenic infection. As HBD-2 has been shown to control growth of M. tuberculosis and has chemotactic activity, our results suggest that HBD-2 induction by M. tuberculosis may have a role in the pathogenesis of human tuberculosis.

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Eisenhut, Michael, Dougal S. Hargreaves, Anne Scott, David Housley, Andrew Walters, and Rohinton Mulla. "Determination of Urinary Neopterin/Creatinine Ratio to Distinguish Active Tuberculosis from Latent Mycobacterium tuberculosis Infection." Journal of Biomarkers 2016 (June 28, 2016): 1–6. http://dx.doi.org/10.1155/2016/5643853.

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Background. Biomarkers to distinguish latent from active Mycobacterium (M.) tuberculosis infection in clinical practice are lacking. The urinary neopterin/creatinine ratio can quantify the systemic interferon-gamma effect in patients with M. tuberculosis infection. Methods. In a prospective observational study, urinary neopterin levels were measured by enzyme linked immunosorbent assay in patients with active tuberculosis, in people with latent M. tuberculosis infection, and in healthy controls and the urinary neopterin/creatinine ratio was calculated. Results. We included a total of 44 patients with M. tuberculosis infection and nine controls. 12 patients had active tuberculosis (8 of them culture-confirmed). The median age was 15 years (range 4.5 to 49). Median urinary neopterin/creatinine ratio in patients with active tuberculosis was 374.1 micromol/mol (129.0 to 1072.3), in patients with latent M. tuberculosis infection it was 142.1 (28.0 to 384.1), and in controls it was 146.0 (40.3 to 200.0), with significantly higher levels in patients with active tuberculosis (p<0.01). The receiver operating characteristics curve had an area under the curve of 0.84 (95% CI 0.70 to 0.97) (p<0.01). Conclusions. Urinary neopterin/creatinine ratios are significantly higher in patients with active tuberculosis compared to patients with latent infection and may be a significant predictor of active tuberculosis in patients with M. tuberculosis infection.

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Wijaya, Chandra, and Fatmawati Fatmawati. "Peranan Sel Sistem Imun Alamiah Pada Infeksi Mycobacterium tuberculosis." Jurnal Ilmu Kedokteran (Journal of Medical Science) 16, no. 2 (October 20, 2022): 71. http://dx.doi.org/10.26891/jik.v16i2.2022.71-78.

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Mycobacterium tuberculosis infection which causes tuberculosis is still a major health problem worldwide due to high morbidity and mortality, where in 2018 tuberculosis caused 1.5 million deaths. The degree of pulmonary tuberculosis varies from mild infiltration, chronic infection, cavity formation to severe and destructive tuberculosis. The difference in the degree of pulmonary tuberculosis is influenced by the response of the immune system to M. tuberculosis. When M. tuberculosis infects the lungs, the human immune system will carry out a series of processes to limit the spread and replication of bacteria. The immune system against M. tuberculosis consists of an innate immune system involving cellular components such as macrophages, neutrophils, Natural Killer (NK cells), dendritic cells and upper respiratory epithelium and an acquired immune response which is mainly mediated by T lymphocyte cells of host that is responsible for recognizing and controlling invasion by pathogens. This review will describe the role of natural immune system cells in M. tuberculosis infection. In addition, a complete description of M. tuberculosis infection will also be discussed to increase understanding of the role of natural immune system cells in M. tuberculosis infection.

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Natarajan, Krishnamurthy, Manikuntala Kundu, Pawan Sharma, and Joyoti Basu. "Innate immune responses to M. tuberculosis infection." Tuberculosis 91, no. 5 (September 2011): 427–31. http://dx.doi.org/10.1016/j.tube.2011.04.003.

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Muflihah, Heni, Manuela Flórido, Leon C. W. Lin, Yingju Xia, James A. Triccas, John Stambas, and Warwick J. Britton. "Boosting BCG with recombinant influenza A virus tuberculosis vaccines increases pulmonary T cell responses but not protection against Mycobacterium tuberculosis infection." PLOS ONE 16, no. 11 (November 18, 2021): e0259829. http://dx.doi.org/10.1371/journal.pone.0259829.

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The current Mycobacterium bovis BCG vaccine provides inconsistent protection against pulmonary infection with Mycobacterium tuberculosis. Immunity induced by subcutaneous immunization with BCG wanes and does not promote early recruitment of T cell to the lungs after M. tuberculosis infection. Delivery of Tuberculosis (TB) vaccines to the lungs may increase and prolong immunity at the primary site of M. tuberculosis infection. Pulmonary immunization with recombinant influenza A viruses (rIAVs) expressing an immune-dominant M. tuberculosis CD4+ T cell epitope (PR8-p25 and X31-p25) stimulates protective immunity against lung TB infection. Here, we investigated the potential use of rIAVs to improve the efficacy of BCG using simultaneous immunization (SIM) and prime-boost strategies. SIM with parenteral BCG and intranasal PR8-p25 resulted in equivalent protection to BCG alone against early, acute and chronic M. tuberculosis infection. Boosting BCG with rIAVs increased the frequency of IFN-γ-secreting specific T cells (p<0.001) and polyfunctional CD4+ T cells (p<0.05) in the lungs compared to the BCG alone, however, this did not result in a significant increase in protection against M. tuberculosis compared to BCG alone. Therefore, sequential pulmonary immunization with these rIAVs after BCG increased M. tuberculosis-specific memory T cell responses in the lung, but not protection against M. tuberculosis infection.

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Zuliartha, Novaily, Ridwan M. Daulay, Melda Deliana, Wisman Dalimunthe, and Rini Savitri Daulay. "Association between passive smoking and Mycobacterium tuberculosis infection in children with household TB contact." Paediatrica Indonesiana 55, no. 1 (March 1, 2015): 29. http://dx.doi.org/10.14238/pi55.1.2015.29-34.

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Background Tuberculosis (TB) and cigarette consumption are relatively high in Indonesia. Passive smoking may increase the risk of infection and disease in adults and children exposed to TB. An association between passive smoking and Mycobacterium tuberculosis infection in children has not been well documented. Objective To assess for an association between passive smoking and M. tuberculosis infection in children who had household contact with a TB patient. Methods This cross-sectional study was conducted in February and March 2011. Children aged 5 to 18 years who had household contact with a TB patient underwent tuberculin testing for M. tuberculosis infection. Subjects were divided into two groups: those exposed to passive smoke and those not exposed to passive smoke. Chi-square test was used to assess for an association between passive smoking and M. tuberculosis infection. Results There were 140 children enrolled in this study, with 70 exposed to passive smoke and 70 not exposed to passive smoke. Prevalence of M. tuberculosis infection was significantly higher in the passive smoking group than in those not exposed to passive smoke [81.4% and 52.9%, respectively, (P= 0.0001)]. In the passive smoking group there were significant associations between nutritional state, paternal and maternal education, and M. tuberculosis infection. But no associations were found between M. tuberculosis infection and familial income or BCG vaccination. Conclusion Among children who had household contact with a TB patient, they who exposed to passive smoke are more likely to have M. tuberculosis infection compared to they who not exposed to passive smoke.

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Capuano, Saverio V., Denise A. Croix, Santosh Pawar, Angelica Zinovik, Amy Myers, Philana L. Lin, Stephanie Bissel, Carl Fuhrman, Edwin Klein, and JoAnne L. Flynn. "Experimental Mycobacterium tuberculosis Infection of Cynomolgus Macaques Closely Resembles the Various Manifestations of Human M. tuberculosis Infection." Infection and Immunity 71, no. 10 (October 2003): 5831–44. http://dx.doi.org/10.1128/iai.71.10.5831-5844.2003.

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ABSTRACT Nonhuman primates were used to develop an animal model that closely mimics human Mycobacterium tuberculosis infection. Cynomolgus macaques were infected with low doses of virulent M. tuberculosis via bronchoscopic instillation into the lung. All monkeys were successfully infected, based on tuberculin skin test conversion and peripheral immune responses to M. tuberculosis antigens. Progression of infection in the 17 monkeys studied was variable. Active-chronic infection, observed in 50 to 60% of monkeys, was characterized by clear signs of infection or disease on serial thoracic radiographs and in other tests and was typified by eventual progression to advanced disease. Approximately 40% of monkeys did not progress to disease in the 15 to 20 months of study, although they were clearly infected initially. These monkeys had clinical characteristics of latent tuberculosis in humans. Low-dose infection of cynomolgus macaques appears to represent the full spectrum of human M. tuberculosis infection and will be an excellent model for the study of pathogenesis and immunology of this infection. In addition, this model will provide an opportunity to study the latent M. tuberculosis infection observed in ∼90% of all infected humans.

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Saukkonen, Jussi J., Beth Bazydlo, Michael Thomas, Robert M. Strieter, Joseph Keane, and Hardy Kornfeld. "β-Chemokines Are Induced by Mycobacterium tuberculosis and Inhibit Its Growth." Infection and Immunity 70, no. 4 (April 2002): 1684–93. http://dx.doi.org/10.1128/iai.70.4.1684-1693.2002.

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ABSTRACT Chemokines (CK) are potent leukocyte activators and chemoattractants and aid in granuloma formation, functions critical for the immune response to Mycobacterium tuberculosis. We hypothesized that infection of alveolar macrophages (AM) with different strains of M. tuberculosis elicits distinct profiles of CK, which could be altered by human immunodeficiency virus (HIV) infection. RANTES, macrophage inflammatory protein-1α (MIP-1α), and MIP-1β were the major β-CK produced in response to M. tuberculosis infection. Virulent M. tuberculosis (H37Rv) induced significantly less MIP-1α than did the avirulent strain (H37Ra), while MIP-1β and RANTES production was comparable for both strains. MIP-1α and MIP-1β were induced by the membrane, but not cytosolic, fraction of M. tuberculosis. M. tuberculosis-induced CK secretion was partly dependent on tumor necrosis factor alpha (TNF-α). AM from HIV-infected individuals produced less TNF-α and MIP-1β than did normal AM in response to either M. tuberculosis strain. We tested the functional significance of decreased β-CK secretion by examining the ability of β-CK to suppress intracellular growth of M. tuberculosis. MIP-1β and RANTES suppressed intracellular growth of M. tuberculosis two- to threefold, a novel finding. Thus, β-CK contribute to the innate immune response to M. tuberculosis infection, and their diminution may promote the intracellular survival of M. tuberculosis.

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Salina, Elena G., and Vadim Makarov. "Mycobacterium tuberculosis Dormancy: How to Fight a Hidden Danger." Microorganisms 10, no. 12 (November 25, 2022): 2334. http://dx.doi.org/10.3390/microorganisms10122334.

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Both latent and active TB infections are caused by a heterogeneous population of mycobacteria, which includes actively replicating and dormant bacilli in different proportions. Dormancy substantially affects M. tuberculosis drug tolerance and TB clinical management due to a significant decrease in the metabolic activity of bacilli, which leads to the complexity of both the diagnosis and the eradication of bacilli. Most diagnostic approaches to latent infection deal with a subpopulation of active M. tuberculosis, underestimating the contribution of dormant bacilli and leading to limited success in the fight against latent TB. Moreover, active TB appears not only as a primary form of infection but can also develop from latent TB, when resuscitation from dormancy is followed by bacterial multiplication, leading to disease progression. To win against latent infection, the identification of the Achilles’ heel of dormant M. tuberculosis is urgently needed. Regulatory mechanisms and metabolic adaptation to growth arrest should be studied using in vitro and in vivo models that adequately imitate latent TB infection in macroorganisms. Understanding the mechanisms underlying M. tuberculosis dormancy and resuscitation may provide clues to help control latent infection, reduce disease severity in patients, and prevent pathogen transmission in the population.

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Kinsella, Rachel L., Jacqueline M. Kimmey, Asya Smirnov, Reilly Woodson, Margaret R. Gaggioli, Sthefany M. Chavez, Darren Kreamalmeyer, and Christina L. Stallings. "Autophagy prevents early proinflammatory responses and neutrophil recruitment during Mycobacterium tuberculosis infection without affecting pathogen burden in macrophages." PLOS Biology 21, no. 6 (June 15, 2023): e3002159. http://dx.doi.org/10.1371/journal.pbio.3002159.

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The immune response to Mycobacterium tuberculosis infection determines tuberculosis disease outcomes, yet we have an incomplete understanding of what immune factors contribute to a protective immune response. Neutrophilic inflammation has been associated with poor disease prognosis in humans and in animal models during M. tuberculosis infection and, therefore, must be tightly regulated. ATG5 is an essential autophagy protein that is required in innate immune cells to control neutrophil-dominated inflammation and promote survival during M. tuberculosis infection; however, the mechanistic basis for how ATG5 regulates neutrophil recruitment is unknown. To interrogate what innate immune cells require ATG5 to control neutrophil recruitment during M. tuberculosis infection, we used different mouse strains that conditionally delete Atg5 in specific cell types. We found that ATG5 is required in CD11c+ cells (lung macrophages and dendritic cells) to control the production of proinflammatory cytokines and chemokines during M. tuberculosis infection, which would otherwise promote neutrophil recruitment. This role for ATG5 is autophagy dependent, but independent of mitophagy, LC3-associated phagocytosis, and inflammasome activation, which are the most well-characterized ways that autophagy proteins regulate inflammation. In addition to the increased proinflammatory cytokine production from macrophages during M. tuberculosis infection, loss of ATG5 in innate immune cells also results in an early induction of TH17 responses. Despite prior published in vitro cell culture experiments supporting a role for autophagy in controlling M. tuberculosis replication in macrophages, the effects of autophagy on inflammatory responses occur without changes in M. tuberculosis burden in macrophages. These findings reveal new roles for autophagy proteins in lung resident macrophages and dendritic cells that are required to suppress inflammatory responses that are associated with poor control of M. tuberculosis infection.

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Fieweger, Wilburn, and VanderVen. "Comparing the Metabolic Capabilities of Bacteria in the Mycobacterium tuberculosis Complex." Microorganisms 7, no. 6 (June 18, 2019): 177. http://dx.doi.org/10.3390/microorganisms7060177.

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Pathogenic mycobacteria are known for their ability to maintain persistent infections in various mammals. The canonical pathogen in this genus is Mycobacterium tuberculosis and this bacterium is particularly successful at surviving and replicating within macrophages. Here, we will highlight the metabolic processes that M. tuberculosis employs during infection in macrophages and compare these findings with what is understood for other pathogens in the M. tuberculosis complex.

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Gallegos, Alena M., Eric G. Pamer, and Michael S. Glickman. "Delayed protection by ESAT-6–specific effector CD4+ T cells after airborne M. tuberculosis infection." Journal of Experimental Medicine 205, no. 10 (September 8, 2008): 2359–68. http://dx.doi.org/10.1084/jem.20080353.

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Mycobacterium tuberculosis infection induces complex CD4 T cell responses that include T helper type 1 (Th1) cells and regulatory T cells. Although Th1 cells control infection, they are unable to fully eliminate M. tuberculosis, suggesting that Th1-mediated immunity is restrained from its full sterilizing potential. Investigation into T cell–mediated defense is hindered by difficulties in expanding M. tuberculosis–specific T cells. To circumvent this problem, we cloned CD4+ T cells from M. tuberculosis–infected B6 mice and generated transgenic mice expressing a T cell receptor specific for the immunodominant antigen early secreted antigenic target 6 (ESAT-6). Adoptively transferred naive ESAT-6–specific CD4+ T cells are activated in pulmonary lymph nodes between 7 and 10 d after aerosol infection and undergo robust expansion before trafficking to the lung. Adoptive transfer of activated ESAT-6–specific Th1 cells into naive recipients before aerosol M. tuberculosis infection dramatically enhances resistance, resulting in 100-fold fewer bacteria in infected lungs. However, despite large numbers of Th1 cells in the lungs of mice at the time of M. tuberculosis challenge, protection was not manifested until after 7 d following infection. Our results demonstrate that pathogen-specific Th1 cells can provide protection against inhaled M. tuberculosis, but only after the first week of infection.

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Antonenko, Kate, Valentin Kresyun, and Peter Antonenko. "Mutations leading to drug-resistant Mycobacterium tuberculosis infection in Ukraine." Open Medicine 5, no. 1 (February 1, 2010): 30–35. http://dx.doi.org/10.2478/s11536-009-0114-6.

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AbstractThe goal of this research was detection of the drug-resistance level of Mycobacterium tuberculosis infection in the Odesa region of Southwest Ukraine, investigation of the level of mutation in katG and rpoB genes for M. tuberculosis with polymerase chain reaction (PCR), and spread of these mutations in different groups of patients with tuberculosis. An extremely high level of primary and acquired resistance of M. tuberculosis to first-line antituberculosis drugs has been found in the Southwest region of Ukraine. The PCR method has proved to have high sensitivity in the detection of mutations in katG and rpoB genes. The data showed significant spreading of M. tuberculosis strains with mutations in katG and rpoB genes in penitentiaries and an increased level of these mutations during tuberculosis treatment. The presence of mutations in rpoB and katG genes was associated with a more severe course of tuberculosis, increased risk of treatment default, persistence of positive smears on microscopy at discharge, and poor closing of tuberculous cavities. Extremely high level of mutations in the rpoB and katG genes of M. tuberculosis was observed in Beijing family strains. Our findings support the capability of the PCR method to detect M. tuberculosis that is resistant to drugs such as isoniazid and rifampicin.

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Saralahti, Anni K., Meri I. E. Uusi-Mäkelä, Mirja T. Niskanen, and Mika Rämet. "Integrating fish models in tuberculosis vaccine development." Disease Models & Mechanisms 13, no. 8 (August 1, 2020): dmm045716. http://dx.doi.org/10.1242/dmm.045716.

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ABSTRACTTuberculosis is a chronic infection by Mycobacterium tuberculosis that results in over 1.5 million deaths worldwide each year. Currently, there is only one vaccine against tuberculosis, the Bacillus Calmette–Guérin (BCG) vaccine. Despite widespread vaccination programmes, over 10 million new M. tuberculosis infections are diagnosed yearly, with almost half a million cases caused by antibiotic-resistant strains. Novel vaccination strategies concentrate mainly on replacing BCG or boosting its efficacy and depend on animal models that accurately recapitulate the human disease. However, efforts to produce new vaccines against an M. tuberculosis infection have encountered several challenges, including the complexity of M. tuberculosis pathogenesis and limited knowledge of the protective immune responses. The preclinical evaluation of novel tuberculosis vaccine candidates is also hampered by the lack of an appropriate animal model that could accurately predict the protective effect of vaccines in humans. Here, we review the role of zebrafish (Danio rerio) and other fish models in the development of novel vaccines against tuberculosis and discuss how these models complement the more traditional mammalian models of tuberculosis.

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Gandotra, Sheetal, Sihyug Jang, Peter J. Murray, Padmini Salgame, and Sabine Ehrt. "Nucleotide-Binding Oligomerization Domain Protein 2-Deficient Mice Control Infection with Mycobacterium tuberculosis." Infection and Immunity 75, no. 11 (August 20, 2007): 5127–34. http://dx.doi.org/10.1128/iai.00458-07.

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ABSTRACT Nucleotide-binding oligomerization domain proteins (NODs) are modular cytoplasmic proteins implicated in the recognition of peptidoglycan-derived molecules. NOD2 has recently been shown to be important for host cell cytokine responses to Mycobacterium tuberculosis, to synergize with Toll-like receptor 2 (TLR2) in mediating these responses, and thus to serve as a nonredundant recognition receptor for M. tuberculosis. Here, we demonstrate that macrophages and dendritic cells from NOD2-deficient mice were impaired in the production of proinflammatory cytokines and nitric oxide following infection with live, virulent M. tuberculosis. Mycolylarabinogalactan peptidoglycan (PGN), the cell wall core of M. tuberculosis, stimulated macrophages to release tumor necrosis factor (TNF) and interleukin-12p40 in a partially NOD2-dependent manner, and M. tuberculosis PGN required NOD2 for the optimal induction of TNF. However, NOD2-deficient mice were no more susceptible to infection with virulent M. tuberculosis than wild-type mice: they controlled the replication of M. tuberculosis in lung, spleen, and liver as well as wild-type mice, and both genotypes displayed similar lung pathologies. In addition, mice doubly deficient for NOD2 and TLR2 were similarly able to control an M. tuberculosis infection. Thus, NOD2 appears to participate in the recognition of M. tuberculosis by antigen-presenting cells in vitro yet is dispensable for the control of the pathogen during in vivo infection.

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Kelly, Deirdre M., Annemieke M. C. ten Bokum, Seonadh M. O'Leary, Mary P. O'Sullivan, and Joseph Keane. "Bystander Macrophage Apoptosis after Mycobacterium tuberculosis H37Ra Infection." Infection and Immunity 76, no. 1 (October 22, 2007): 351–60. http://dx.doi.org/10.1128/iai.00614-07.

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ABSTRACT Human macrophages infected with Mycobacterium tuberculosis may undergo apoptosis. Macrophage apoptosis contributes to the innate immune response against M. tuberculosis by containing and limiting the growth of mycobacteria and also by depriving the bacillus of its niche cell. Apoptosis of infected macrophages is well documented; however, bystander apoptosis of uninfected macrophages has not been described in the setting of M. tuberculosis. We observed that uninfected human macrophages underwent significant bystander apoptosis 48 and 96 h after they came into contact with macrophages infected with avirulent M. tuberculosis. The bystander apoptosis was significantly greater than the background apoptosis observed in uninfected control cells cultured for the same length of time. There was no evidence of the involvement of tumor necrosis factor alpha, Fas, tumor necrosis factor-related apoptosis-inducing ligand, transforming growth factor β, Toll-like receptor 2, or MyD88 in contact-mediated bystander apoptosis. This newly described phenomenon may further limit the spread of M. tuberculosis by eliminating the niche cells on which the bacillus relies.

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Dobos, Karen M., Ellen A. Spotts, Frederick D. Quinn, and C. Harold King. "Necrosis of Lung Epithelial Cells during Infection withMycobacterium tuberculosis Is Preceded by Cell Permeation." Infection and Immunity 68, no. 11 (November 1, 2000): 6300–6310. http://dx.doi.org/10.1128/iai.68.11.6300-6310.2000.

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ABSTRACT Mycobacterium tuberculosis establishes infection, progresses towards disease, and is transmitted from the alveolus of the lung. However, the role of the alveolar epithelium in any of these pathogenic processes of tuberculosis is unclear. In this study, lung epithelial cells (A549) were used as a model in which to examine cytotoxicity during infection with either virulent or avirulent mycobacteria in order to further establish the role of the lung epithelium during tuberculosis. Infection of A549 cells with M. tuberculosis strains Erdman and CDC1551 demonstrated significant cell monolayer clearing, whereas infection with eitherMycobacterium bovis BCG or Mycobacterium smegmatis LR222 did not. Clearing of M. tuberculosis-infected A549 cells correlated to necrosis, not apoptosis. Treatment of M. tuberculosis-infected A549 cells with streptomycin, but not cycloheximide, demonstrated a significant reduction in the necrosis of A549 cell monolayers. This mycobacterium-induced A549 necrosis did not correlate to higher levels of intracellular or extracellular growth by the mycobacteria during infection. Staining of infected cells with propidium iodide demonstrated that M. tuberculosis induced increased permeation of A549 cell membranes within 24 h postinfection. Quantitation of lactate dehydrogenase (LDH) release from infected cells further demonstrated that cell permeation was specific to M. tuberculosis infection and correlated to A549 cellular necrosis. Inactivated M. tuberculosis or its subcellular fractions did not result in A549 necrosis or LDH release. These studies demonstrate that lung epithelial cell cytotoxicity is specific to infection by virulent mycobacteria and is caused by cellular necrosis. This necrosis is not a direct correlate of mycobacterial growth or of the expression of host cell factors, but is preceded by permeation of the A549 cell membrane and requires infection with live bacilli.

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Yanti, Budi, Soetjipto Soetjipto, Ni Made Mertaniasih, and Muhammad Amin. "Clinical and Demographic Characteristics Differences between M. tuberculosis and M. bovis Infection in Bronchoalveolar Lavage Pulmonary TB Patients, Indonesia." Jurnal Respirologi Indonesia 39, no. 4 (October 3, 2019): 238–44. http://dx.doi.org/10.36497/jri.v39i4.76.

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Background: Some species of the Mycobacterium tuberculosis complex (MTBC) which can cause tuberculosis, particularly M. tuberculosis and M. bovis, may have different virulence property and therefore associated with various clinical severity in tuberculosis (TB) patients. The aim of this study was to determine the differences in clinical and demographic characteristics between M. tuberculosis and M. bovis infection among Indonesian TB patients. Methods: Thirty-one new and active TB patients were confirmed to have acid fast bacilli (AFB) sputum positive and/or Xpert MTB/RIF positive for M. tuberculosis from Dr. Soewandhie Hospital, Surabaya, Indonesia. Interviews were conducted to record the clinical and demographics required. The MTBC were isolated from bronchoalveolar lavage fluid (BALF) and determined by primer-specific PCR targeting TbD1 and RD9 region gene. The degree of lung tissue damage was classified using NICE Scoring System. Results: The MTBC were detected in all patients on whom 19 and 12 isolates were classified as M. tuberculosis and M. bovis respectively. There was a different on 74.2% of productive age subjects (21-50 years) with M. tuberculosis infection (P

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26

Lin, May Young, T. B. K. Reddy, Sandra M. Arend, Annemieke H. Friggen, Kees L. M. C. Franken, Krista E. van Meijgaarden, Marleen J. C. Verduyn, Gary K. Schoolnik, Michel R. Klein, and Tom H. M. Ottenhoff. "Cross-Reactive Immunity to Mycobacterium tuberculosis DosR Regulon-Encoded Antigens in Individuals Infected with Environmental, Nontuberculous Mycobacteria." Infection and Immunity 77, no. 11 (September 8, 2009): 5071–79. http://dx.doi.org/10.1128/iai.00457-09.

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ABSTRACT Mycobacterium tuberculosis DosR regulon-encoded antigens are highly immunogenic in M. tuberculosis-infected humans and are associated with latent tuberculosis infection. We have investigated the hypothesis that infection with or exposure to nontuberculous mycobacteria (NTM) can induce cross-reactive immunity to M. tuberculosis DosR regulon-encoded antigens since responsiveness has been observed in non-M. tuberculosis-exposed but purified protein derivative-responsive individuals. M. tuberculosis DosR regulon-encoded antigen-specific T-cell responses were studied in peripheral blood mononuclear cells (PBMCs) of NTM-infected/exposed individuals. BLASTP was used to determine the presence of M. tuberculosis DosR regulon-encoded protein orthologs among environmental mycobacteria and nonmycobacteria. Significant gamma interferon production was observed in PBMCs from NTM-infected/exposed individuals in response to M. tuberculosis DosR regulon-encoded antigens. DosR regulon-encoded protein orthologs were prominently present in tuberculous and environmental mycobacteria and surprisingly also in nonmycobacteria. The ubiquitous presence of the highly conserved DosR master regulator protein Rv3133c suggests that this is a general adaptive bacterial response regulator. We report a first series of M. tuberculosis antigens to which cross-reactive immunity is induced by NTM infection/exposure. The high conservation of M. tuberculosis DosR regulon-encoded antigens most likely enables them to induce cross-reactive T-cell responses.

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Sharma, Sumedha, Romica Latawa, Ajay Wanchu, and Indu Verma. "Differential diagnosis of disseminated Mycobacterium avium and Mycobacterium tuberculosis infection in HIV patients using duplex PCR." Future Microbiology 16, no. 3 (February 2021): 135–42. http://dx.doi.org/10.2217/fmb-2020-0091.

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Background: Disseminated Mycobacterium avium complex (MAC) and Mycobacterium tuberculosis infections have almost similar clinical presentations but require different therapeutic management. Materials & methods: A duplex PCR was designed based on the sequence variation between the genes encoding catalase-peroxidase (KatG) of M. avium complex and M. tuberculosis, so as to discriminate MAC, M. tuberculosis and mixed mycobacterial (MAC + M. tuberculosis) infections in HIV patients. Results: An accurate, single-step differential diagnosis of disseminated mycobacterial infections in HIV patients was achieved with specific detection of a single band each for M. avium (120 bp) and M. tuberculosis (90 bp) and two bands for the mixed (120 and 90 bp) infections. Conclusion: katG gene-based duplex PCR can facilitate quick differential diagnosis of disseminated MAC and M. tuberculosis infections in HIV patients.

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Yang, Chao-Tsung, Laura E. Swaim, and Lalita Ramakrishnan. "Mechanism of M-CSF pathway-mediated innate resistance to tuberculosis (134.76)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 134.76. http://dx.doi.org/10.4049/jimmunol.182.supp.134.76.

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Abstract The outcome of mycobacterial infections is determined by interactions between host and bacterial factors yet only very few host factors that affect the susceptibility to the infections are known. In particular, there has been an increasing appreciation that both innate immunity and hematopoietic growth factors such as M-CSF play important roles in modulating tuberculosis. The Ramakrishnan laboratory has established a model for mycobacterial pathogenesis using Mycobacterium marinum (Mm) in the optically transparent and genetically tractable zebrafish. This model allows us to dissect the host cellular and genetic mechanisms that regulate macrophage function during infection. We have found that zebrafish with mutations in the M-CSF-receptor, fms, are hypersusceptible to Mm. M-CSF has pleitropic effects on macrophage development and function. To determine its mechanism of resistance in infection, we performed a step-wise comparison of infection in wildtype and fms-mutant fish. We found that initial macrophage production, as well as macrophage migration to infection sites, phagocytosis and microbicidal capacity were all normal in the fms mutants. Hypersusceptibility became apparent only after granulomas had formed. We are currently testing the hypothesis that the M-CSF pathway is required for macrophage replenishment during infection to maintain granuloma integrity and retain the bacteria within a more restrictive intracellular niche. This study may shed light on the genetics of macrophage homeostasis during mycobacterial infection.

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Waters, W. R., A. O. Whelan, K. P. Lyashchenko, R. Greenwald, M. V. Palmer, B. N. Harris, R. G. Hewinson, and H. M. Vordermeier. "Immune Responses in Cattle Inoculated with Mycobacterium bovis, Mycobacterium tuberculosis, or Mycobacterium kansasii." Clinical and Vaccine Immunology 17, no. 2 (December 9, 2009): 247–52. http://dx.doi.org/10.1128/cvi.00442-09.

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ABSTRACT Cattle were inoculated with Mycobacterium bovis, Mycobacterium tuberculosis, or Mycobacterium kansasii to compare the antigen-specific immune responses to various patterns of mycobacterial disease. Disease expression ranged from colonization with associated pathology (M. bovis infection) and colonization without pathology (M. tuberculosis infection) to no colonization or pathology (M. kansasii infection). Delayed-type hypersensitivity and gamma interferon responses were elicited by each mycobacterial inoculation; however, the responses by the M. bovis- and M. tuberculosis-inoculated animals exceeded those of the M. kansasii-inoculated animals. Specific antibody responses were detected in all M. tuberculosis- and M. bovis-inoculated cattle 3 weeks after inoculation. From 6 to 16 weeks after M. tuberculosis inoculation, the antibody responses waned, whereas the responses persisted with M. bovis infection. With M. kansasii inoculation, initial early antibody responses waned by 10 weeks after inoculation and then increased 2 weeks after the injection of purified protein derivative for the skin test at 18 weeks after challenge. These findings indicate that antibody responses are associated with the antigen burden rather than the pathology, cellular immune responses to tuberculin correlate with infection but not necessarily with the pathology or bacterial burden, and exposure to mycobacterial antigens may elicit an antibody response in a presensitized animal.

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Kayukova, S. I., A. E. Panova, M. M. Averbakh, B. V. Nikonenko, A. N. Gracheva, N. I. Kompantseva, A. L. Bayrakova, A. A. Kazyulina, and A. S. Vinokurov. "State of the Lung Microbiota in С57bl/6 Mice in the Experimental Tuberculosis Model." Tuberculosis and Lung Diseases 101, no. 2 (April 28, 2023): 94–99. http://dx.doi.org/10.58838/2075-1230-2023-101-2-94-99.

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The objective: to study the changes in the lung microbiota in inbred C57BL/6 mice after aerogenic infection with M. tuberculosis in an experimental tuberculosis model.Subjects and Methods. This study was carried out on 20 female mice of inbred line C57BL/6 weighing 20-22 grams which were infected in a Glas-Col aerosol chamber (USA) with the culture of M. tuberculosis of virulent strain H37Rv at the dose of 400 CFU/lung. Morphological and microbiological assessment of the lungs state was performed before (day 0) (n=5) and 7 (n=5), 30 (n=5) and 60 (n=5) days after the infection. The results obtained were subjected to statistical processing using ANOVA test and Student t-test.Results. 7, 30, and 60 days after aerosol infection with M. tuberculosis against the background of successive morphological and microbiological changes typical of the experimental tuberculosis model, we established an imbalance of bacterial population in the lung microbiota. Before infection with M. tuberculosis, a scanty biotope was recorded with a predominance of lactobacilli –Lactobacillus murinus, Lactobacillus apodeme. 7, 30 and 60 days after infection with M. tuberculosis, consistent changes were recorded, such as increase in the number and diversity of the bacterial population. The most indicative markers of the recorded imbalance were: Streptococcus thoraltensis, Streptococcus acidominiminus, Arthrobacter crystallopoietes, Staphylococcus hominis, Micrococcus luteus.Conclusion. Tuberculosis infection is a significant factor affecting the state of the lung microbiota. With increased duration of the infection with M. tuberculosis, imbalance of the bacterial flora is formed in the lungs of C57BL/6 mice, accompanied by characteristic tissue inflammation and growing mycobacterial load.

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Alvarez, María Alejandra, Patricia Arbelaez, Francisco Ignacio Bastos, Ben Berkhout, Basudev Bhattacharya, Gennady Bocharov, Valery Chereshnev, et al. "Research Priorities for HIV/M. tuberculosis Co-Infection." Open Infectious Diseases Journal 5, no. 1 (March 7, 2011): 14–20. http://dx.doi.org/10.2174/1874279301005010014.

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Alvarez, María Alejandra. "Research Priorities for HIV/M. tuberculosis Co-Infection." Open Infectious Diseases Journal 5, no. 1 (July 6, 2011): 14–20. http://dx.doi.org/10.2174/1874279301105010014.

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Pande, Tarun K., Sujata Hiran, V. V. B. Rao, Sidhartha Pani, and K. A. Vishwanathan. "Primary lingual tuberculosis caused by M. bovis infection." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 80, no. 2 (August 1995): 172–74. http://dx.doi.org/10.1016/s1079-2104(05)80197-0.

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Zhang, Jing, Yan-Qing Ye, Yong Wang, Ping-Zheng Mo, Qiao-Yang Xian, Yan Rao, Rong Bao, et al. "M. tuberculosis H37Rv Infection of Chinese Rhesus Macaques." Journal of Neuroimmune Pharmacology 6, no. 3 (October 12, 2010): 362–70. http://dx.doi.org/10.1007/s11481-010-9245-4.

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Yoon, Hyung Seok, Eun Joo Lee, Jung Yeon Lee, Gyu Rak Chon, Sang Ho Lee, and Se Jin Kim. "Organizing pneumonia associated with M ycobacterium tuberculosis infection." Respirology Case Reports 3, no. 4 (November 12, 2015): 128–31. http://dx.doi.org/10.1002/rcr2.135.

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Kashino, Suely S., Pamela Ovendale, Angelo Izzo, and Antonio Campos-Neto. "Unique Model of Dormant Infection for Tuberculosis Vaccine Development." Clinical and Vaccine Immunology 13, no. 9 (September 2006): 1014–21. http://dx.doi.org/10.1128/cvi.00120-06.

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ABSTRACT Most individuals exposed to Mycobacterium tuberculosis become infected but hinder the infectious process in dormant foci, known as latent tuberculosis. This limited infection usually stimulates strong T-cell responses, which provide lifelong resistance to tuberculosis. However, latent tuberculosis is still poorly understood, particularly because of the lack of a reliable animal model of dormant infection. Here we show that inoculation of mice with a unique streptomycin-auxotrophic mutant of Mycobacterium tuberculosis recapitulates dormant infection. The mutant grows unimpaired in the presence of streptomycin and no longer grows but remains viable for long periods of time after substrate removal, shifting from the log growth phase to the latent stage, as indicated by augmented production of α-crystallin. Mice challenged with the mutant and inoculated with streptomycin for ∼3 weeks developed a limited infection characterized by a low bacteriological burden and the presence of typical granulomas. After substrate withdrawal, the infection was hindered but few microorganisms remained viable (dormant) in the animals' tissues for at least 6 months. In addition, the animals developed both potent T-cell responses to M. tuberculosis antigens, such as early culture filtrate, Ag85B, and ESAT-6, and resistance to reinfection with virulent M. tuberculosis. Therefore, infection of mice or other animals (e.g., guinea pigs) with M. tuberculosis strain 18b constitutes a simple and attractive animal model for evaluation of antituberculosis vaccines in the context of an M. tuberculosis-presensitized host, a prevailing condition among humans in need of a vaccine.

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Xing, Xiaoming, Cuiyun Zhang, Jie Zhou, Qian Jin, and Qinfang Zheng. "BAG2-activated cell autophagy and mir-27b dynamic regulation mechanism during Mycobacterium tuberculosis infection." Cellular and Molecular Biology 67, no. 5 (February 4, 2022): 38–44. http://dx.doi.org/10.14715/cmb/2021.67.5.5.

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Tuberculosis is a highly contagious infectious disease. Mycobacterium tuberculosis infection is the main cause of tuberculosis. During the infection of M. tuberculosis, the expression of the resistance gene BAG2 will change, and miR-27b will play a certain role in dynamic regulation. The purpose of this article is to explore in-depth the effect of BAG2 on cell autophagy during M. tuberculosis infection and the dynamic regulatory mechanism of miR-27b on BAG2 activated cell autophagy. Fifty rats were used as experimental subjects, and M. tuberculosis strains H37Ra and H37Rv were implanted into the rats. Fluorescence quantitative PCR was used to detect the dynamic changes of BAG2 and miR-27b expression levels in rats and the regulatory effect of miR-27b on BAG2, and the effect of changes in BAG2 expression levels on cell autophagy was studied by immunoblotting. The results showed that after M. tuberculosis-infected macrophages, the expression level of BAG2 decreased from (284.24±6.31) to (156.48.24±4.49), and the expression level of miR-27b was increased from (43.72±3.35) to (78.35± 4.17), the apoptosis rate increased by 17.8%, and the autophagy rate increased by 20.6%. Therefore, it can be seen that the up-regulation of miR-27b expression level during M. tuberculosis infection will inhibit BAG2 expression, thereby promoting cell autophagy and apoptosis to reduce the survival rate of M. tuberculosis.

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Lazarevic, Vanja, David J. Yankura, Sherrie J. Divito, and JoAnne L. Flynn. "Induction of Mycobacterium tuberculosis-Specific Primary and Secondary T-Cell Responses in Interleukin-15-Deficient Mice." Infection and Immunity 73, no. 5 (May 2005): 2910–22. http://dx.doi.org/10.1128/iai.73.5.2910-2922.2005.

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ABSTRACT Several studies have provided evidence that interleukin-15 (IL-15) can enhance protective immune responses against Mycobacterium tuberculosis infection. However, the effects of IL-15 deficiency on the functionality of M. tuberculosis-specific CD4 and CD8 T cells are unknown. In this study, we investigated the generation and maintenance of effector and memory T-cell responses following M. tuberculosis infection of IL-15−/− mice. IL-15−/− mice had slightly higher bacterial numbers during chronic infection, which were accompanied by an increase in gamma interferon (IFN-γ)-producing CD4 and CD8 T cells. There was no evidence of increased apoptosis or a defect in proliferation of CD8 effector T cells following M. tuberculosis infection. The induction of cytotoxic and IFN-γ CD8 T-cell responses was normal in the absence of IL-15 signaling. The infiltration of CD4 and CD8 T cells into the lungs of “immune” IL-15−/− mice was delayed in response to M. tuberculosis challenge. These findings demonstrate that efficient effector CD4 and CD8 T cells can be developed following M. tuberculosis infection in the absence of IL-15 but that recall T-cell responses may be impaired.

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Pai, Rish K., Meghan E. Pennini, Aaron A. R. Tobian, David H. Canaday, W. Henry Boom, and Clifford V. Harding. "Prolonged Toll-Like Receptor Signaling by Mycobacterium tuberculosis and Its 19-Kilodalton Lipoprotein Inhibits Gamma Interferon-Induced Regulation of Selected Genes in Macrophages." Infection and Immunity 72, no. 11 (November 2004): 6603–14. http://dx.doi.org/10.1128/iai.72.11.6603-6614.2004.

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ABSTRACT Infection of macrophages with Mycobacterium tuberculosis or exposure to M. tuberculosis 19-kDa lipoprotein for >16 h inhibits gamma interferon (IFN-γ)-induced major histocompatibility complex class II (MHC-II) expression by a mechanism involving Toll-like receptors (TLRs). M. tuberculosis was found to inhibit murine macrophage MHC-II antigen (Ag) processing activity induced by IFN-γ but not by interleukin-4 (IL-4), suggesting inhibition of IFN-γ-induced gene regulation. We designed an approach to test the ability of M. tuberculosis-infected cells to respond to IFN-γ. To model chronic infection with M. tuberculosis with accompanying prolonged TLR signaling, macrophages were infected with M. tuberculosis or incubated with M. tuberculosis 19-kDa lipoprotein for 24 h prior to the addition of IFN-γ. Microarray gene expression studies were then used to determine whether prolonged TLR signaling by M. tuberculosis broadly inhibits IFN-γ regulation of macrophage gene expression. Of 347 IFN-γ-induced genes, M. tuberculosis and 19-kDa lipoprotein inhibited induction of 42 and 36%, respectively. Key genes or gene products were also examined by quantitative reverse transcription-PCR and flow cytometry, confirming and extending the results obtained by microarray studies. M. tuberculosis inhibited IFN-γ induction of genes involved in MHC-II Ag processing, Ag presentation, and recruitment of T cells. These effects were largely dependent on myeloid differentiation factor 88, implying a role for TLRs. Thus, prolonged TLR signaling by M. tuberculosis inhibits certain macrophage responses to IFN-γ, particularly those related to MHC-II Ag presentation. This inhibition may promote M. tuberculosis evasion of T-cell responses and persistence of infection in tuberculosis.

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Zahrt, Thomas C., and Vojo Deretic. "An Essential Two-Component Signal Transduction System in Mycobacterium tuberculosis." Journal of Bacteriology 182, no. 13 (July 1, 2000): 3832–38. http://dx.doi.org/10.1128/jb.182.13.3832-3838.2000.

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ABSTRACT The bacterial two-component signal transduction systems regulate adaptation processes and are likely to play a role inMycobacterium tuberculosis physiology and pathogenesis. The previous initial characterization of an M. tuberculosis response regulator from one of these systems,mtrA-mtrB, suggested its transcriptional activation during infection of phagocytic cells. In this work, we further characterized the mtrA response regulator fromM. tuberculosis H37Rv. Inactivation ofmtrA on the chromosome of M. tuberculosisH37Rv was possible only in the presence of plasmid-borne functionalmtrA, suggesting that this response regulator is essential for M. tuberculosis viability. In keeping with these findings, expression of mtrA in M. tuberculosis H37Rv was detectable during in vitro growth, as determined by S1 nuclease protection and primer extension analyses of mRNA levels and mapping of transcript 5′ ends. The mtrAgene was expressed differently in virulent M. tuberculosis and the vaccine strain M. tuberculosis var. bovis BCG during infection of macrophages, as determined by monitoring of mtrA-gfp fusion activity. In M. bovis BCG, mtrA was induced upon entry into macrophages. In M. tuberculosis H37Rv, its expression was constitutive and unchanged upon infection of murine or human monocyte-derived macrophages. In conclusion, these results identify mtrA as an essential response regulator gene in M. tuberculosis which is differentially expressed in virulent and avirulent strains during growth in macrophages.

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Starshinova, Anna A., Igor Kudryavtsev, Anna Malkova, Ulia Zinchenko, Vadim Karev, Dmitry Kudlay, Angela Glushkova, et al. "Molecular and Cellular Mechanisms of M. tuberculosis and SARS-CoV-2 Infections—Unexpected Similarities of Pathogenesis and What to Expect from Co-Infection." International Journal of Molecular Sciences 23, no. 4 (February 17, 2022): 2235. http://dx.doi.org/10.3390/ijms23042235.

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Tuberculosis is still an important medical and social problem. In recent years, great strides have been made in the fight against M. tuberculosis, especially in the Russian Federation. However, the emergence of a new coronavirus infection (COVID-19) has led to the long-term isolation of the population on the one hand and to the relevance of using personal protective equipment on the other. Our knowledge regarding SARS-CoV-2-induced inflammation and tissue destruction is rapidly expanding, while our understanding of the pathology of human pulmonary tuberculosis gained through more the 100 years of research is still limited. This paper reviews the main molecular and cellular differences and similarities caused by M. tuberculosis and SARS-CoV-2 infections, as well as their critical immunological and pathomorphological features. Immune suppression caused by the SARS-CoV-2 virus may result in certain difficulties in the diagnosis and treatment of tuberculosis. Furthermore, long-term lymphopenia, hyperinflammation, lung tissue injury and imbalance in CD4+ T cell subsets associated with COVID-19 could propagate M. tuberculosis infection and disease progression.

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Domenech, Pilar, Hajime Kobayashi, Kristin LeVier, Graham C. Walker, and Clifton E. Barry. "BacA, an ABC Transporter Involved in Maintenance of Chronic Murine Infections with Mycobacterium tuberculosis." Journal of Bacteriology 191, no. 2 (November 7, 2008): 477–85. http://dx.doi.org/10.1128/jb.01132-08.

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ABSTRACT BacA is an inner membrane protein associated with maintenance of chronic infections in several diverse host-pathogen interactions. To understand the function of the bacA gene in Mycobacterium tuberculosis (Rv1819c), we insertionally inactivated this gene and analyzed the resulting mutant for a variety of phenotypes. BacA deficiency in M. tuberculosis did not affect sensitivity to detergents, acidic pH, and zinc, indicating that there was no global compromise in membrane integrity, and a comprehensive evaluation of the major lipid constituents of the cell envelope failed to reveal any significant differences. Infection of mice with this mutant revealed no impact on establishment of infection but a profound effect on maintenance of extended chronic infection and ultimate outcome. As in alphaproteobacteria, deletion of BacA in M. tuberculosis led to increased bleomycin resistance, and heterologous expression of the M. tuberculosis BacA homolog in Escherichia coli conferred sensitivity to antimicrobial peptides. These results suggest a striking conservation of function for BacA-related proteins in transport of a critical molecule that determines the outcome of the host-pathogen interaction.

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Davidow, Amy, Ganga V. Kanaujia, Lanbo Shi, Justin Kaviar, XuDong Guo, Nackmoon Sung, Gilla Kaplan, Dick Menzies, and Maria L. Gennaro. "Antibody Profiles Characteristic of Mycobacterium tuberculosis Infection State." Infection and Immunity 73, no. 10 (October 2005): 6846–51. http://dx.doi.org/10.1128/iai.73.10.6846-6851.2005.

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ABSTRACT The relationship between specific antibody profiles and tuberculosis (TB) state was investigated by measuring serum antibody levels to six Mycobacterium tuberculosis antigens in human subjects grouped into four diagnostic categories: active disease, inactive (past) tuberculosis, latent infection without radiographic chest abnormalities, and infection free. Statistical data analyses showed that the latter two groups were serologically indistinguishable and that active tuberculosis and inactive tuberculosis were characterized by different antibody profiles. Antibodies to the 38-kDa antigen, alanine dehydrogenase, and Rv2626c were associated with active TB, while antibodies to the 16-kDa antigen, ferredoxin A, and ESAT-6 were associated with inactive TB. Thus, the targets of the immune response vary with tuberculosis state. The correlation between bacterial antigen production and infection stage was investigated in mice infected with M. tuberculosis by bacterial transcription profiling. It was found that levels of transcripts encoding the six M. tuberculosis antigens varied during infection. Together, the data indicate that antigen composition of tubercle bacilli varies with stage of infection and that immunoprofiling can distinguish between tuberculosis states.

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Vorkas, Charles Kyriakos, Olivier Levy, Miroslav Skular, Kelin Li, Jeffrey Aubé, and Michael S. Glickman. "Efficient 5-OP-RU-Induced Enrichment of Mucosa-Associated Invariant T Cells in the Murine Lung Does Not Enhance Control of Aerosol Mycobacterium tuberculosis Infection." Infection and Immunity 89, no. 1 (October 19, 2020): e00524-20. http://dx.doi.org/10.1128/iai.00524-20.

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ABSTRACTMucosa-associated invariant T (MAIT) cells are an innate-like T cell subset in mammals that recognize microbial vitamin B metabolites presented by the evolutionarily conserved major histocompatibility complex class I (MHC I)-related molecule, MR1. Emerging data suggest that MAIT cells may be an attractive target for vaccine-induced protection against bacterial infections because of their rapid cytotoxic responses at mucosal services to a widely conserved bacterial ligand. In this study, we tested whether a MAIT cell priming strategy could protect against aerosol Mycobacterium tuberculosis infection in mice. Intranasal costimulation with the lipopeptide Toll-like receptor (TLR)2/6 agonist, Pam2Cys (P2C), and the synthetic MR1 ligand, 5-OP-RU, resulted in robust expansion of MAIT cells in the lung. Although MAIT cell priming significantly enhanced MAIT cell activation and expansion early after M. tuberculosis challenge, these MAIT cells did not restrict M. tuberculosis bacterial load. MAIT cells were depleted by the onset of the adaptive immune response, with decreased detection of granzyme B+ and gamma interferon (IFN-γ)+ MAIT cells relative to that in uninfected P2C/5-OP-RU-treated mice. Decreasing the infectious inoculum, varying the time between priming and aerosol infection, and testing MAIT cell priming in nitric oxide synthase 2 (NOS2)-deficient mice all failed to reveal an effect of P2C/5-OP-RU-induced MAIT cells on M. tuberculosis control. We conclude that intranasal MAIT cell priming in mice induces early MAIT cell activation and expansion after M. tuberculosis exposure, without attenuating M. tuberculosis growth, suggesting that MAIT cell enrichment in the lung is not sufficient to control M. tuberculosis infection.

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Shepelkova, Galina, Vladimir Evstifeev, Mikhail Averbakch Jr., Ilya Sivokozov, Atadzhan Ergeshov, Tatyana Azhikina, and Vladimir Yeremeev. "Small Noncoding RNAs MTS0997 and MTS1338 Affect the Adaptation and Virulence of Mycobacterium tuberculosis." Microbiology Research 12, no. 1 (March 15, 2021): 186–95. http://dx.doi.org/10.3390/microbiolres12010014.

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Tuberculosis (TB) is currently the leading cause of death among bacterial infectious diseases. The spectrum of disease manifestations depends on both host immune responses and the ability of Mycobacterium tuberculosis to resist it. Small non-coding RNAs are known to regulate gene expression; however, their functional role in the relationship of M. tuberculosis with the host is poorly understood. Here, we investigated the effect of small non-coding sRNAs MTS1338 and MTS0997 on M. tuberculosis properties by creating knockout strains. We also assessed the effect of small non-coding RNAs on the survival of wild type and mutant mycobacteria in primary cultures of human alveolar macrophages and the virulence of these strains in a mouse infection model. Wild-type and mutants survived differentially in human alveolar macrophages. Infection of I/St mice with KO M. tuberculosis H37RV strains provided beneficial effects onto major TB phenotypes. We observed attenuated tuberculosis-specific inflammatory responses, including reduced cellular infiltration and decreased granuloma formation in the lungs. Infections caused by KO strains were characterized by significantly lower inflammation of mouse lung tissue and increased survival time of infected animals. Thus, the deletion of MTS0997 and MTS1338 lead to a significant decrease in the virulence of M. tuberculosis.

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Nedeltchev, Gueno G., Tirumalai R. Raghunand, Mandeep S. Jassal, Shichun Lun, Qi-Jian Cheng, and William R. Bishai. "Extrapulmonary Dissemination of Mycobacterium bovis but Not Mycobacterium tuberculosis in a Bronchoscopic Rabbit Model of Cavitary Tuberculosis." Infection and Immunity 77, no. 2 (December 8, 2008): 598–603. http://dx.doi.org/10.1128/iai.01132-08.

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ABSTRACT The rabbit model of tuberculosis is attractive because of its pathophysiologic resemblance to the disease in humans. Rabbits are naturally resistant to infection but may manifest cavitary lung lesions. We describe here a novel approach that utilizes presensitization and bronchoscopic inoculation to reliably produce cavities in the rabbit model. With a fixed inoculum of bacilli, we were able to reproducibly generate cavities by using Mycobacterium bovis Ravenel, M. bovis AF2122, M. bovis BCG, M. tuberculosis H37Rv, M. tuberculosis CDC1551, and the M. tuberculosis CDC1551 ΔsigC mutant. M. bovis infections generated cavitary CFU counts of 106 to 109 bacilli, while non-M. bovis species and BCG yielded CFU counts that ranged from 104 to 108 bacilli. Extrapulmonary dissemination was almost exclusively noted among rabbits infected with M. bovis Ravenel and AF2122. Though all of the species yielded secondary lesions at intrapulmonary sites, M. bovis infections led to the most apparent gross pathology. Using the M. tuberculosis icl and dosR gene expression patterns as molecular sentinels, we demonstrated that both the cavity wall and cavity lumen are microenvironments associated with hypoxia, upregulation of the bacterial dormancy program, and the use of host lipids for bacterial catabolism. This unique cavitary model provides a reliable animal model to study cavity pathogenesis and extrapulmonary dissemination.

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Manabe, Yukari C., Arthur M. Dannenberg, Sandeep K. Tyagi, Christine L. Hatem, Mark Yoder, Samuel C. Woolwine, Bernard C. Zook, M. Louise M. Pitt, and William R. Bishai. "Different Strains of Mycobacterium tuberculosis Cause Various Spectrums of Disease in the Rabbit Model of Tuberculosis." Infection and Immunity 71, no. 10 (October 2003): 6004–11. http://dx.doi.org/10.1128/iai.71.10.6004-6011.2003.

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ABSTRACT The rabbit model of tuberculosis has been used historically to differentiate between Mycobacterium tuberculosis and Mycobacterium bovis based on their relative virulence in this animal host. M. tuberculosis infection in market rabbits is cleared over time, whereas infection with M. bovis results in chronic, progressive, cavitary disease leading to death. Because of the innate resistance of commercial rabbits to M. tuberculosis, 320 to 1,890 log-phase, actively growing inhaled bacilli were required to form one grossly visible pulmonary tubercle at 5 weeks. The range of inhaled doses required to make one tubercle allows us to determine the relative pathogenicities of different strains. Fewer inhaled organisms of the M. tuberculosis Erdman strain were required than of M. tuberculosis H37Rv to produce a visible lesion at 5 weeks. Furthermore, with the Erdman strain, only 7 of 15 rabbits had healed lesions at 16 to 18 weeks; among the other animals, two had chronic, progressive cavitary disease, a phenotype usually seen only with M. bovis infection. Genotypic investigation of the Erdman strain with an H37Rv-based microarray identified gene differences in the RD6 region. Southern blot and PCR structural genetic analysis showed significant differences between M. tuberculosis strains in this region. Correlation of the relative pathogenicity, including disease severity, in the rabbit model with the strain genotype may help identify stage-specific M. tuberculosis genes important in human disease.

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Kamath, Arati B., and Samuel M. Behar. "Anamnestic Responses of Mice following Mycobacterium tuberculosis Infection." Infection and Immunity 73, no. 9 (September 2005): 6110–18. http://dx.doi.org/10.1128/iai.73.9.6110-6118.2005.

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ABSTRACT The anamnestic response is the property of the immune system that makes vaccine development possible. Although the development of a vaccine against Mycobacterium tuberculosis is an important global priority, there are many gaps in our understanding of how immunological memory develops following M. tuberculosis infection or after BCG vaccination. In experiments designed to compare the anamnestic response of susceptible and resistant mouse strains, major histocompatibility complex-matched memory-immune C3.SW-H2b/SnJ and C57BL/6 mice both demonstrated better control of bacterial replication following reinfection with M. tuberculosis than control mice. Nevertheless, this memory response did not appear to have any long-term protective effect for either mouse strain. A greater understanding of the immunological factors that govern the maintenance of immunological memory following exposure to M. tuberculosis will be required to develop an effective vaccine.

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Scanga, Charles A., Vellore P. Mohan, Kathryn Tanaka, David Alland, JoAnne L. Flynn, and John Chan. "The Inducible Nitric Oxide Synthase Locus Confers Protection against Aerogenic Challenge of Both Clinical and Laboratory Strains of Mycobacterium tuberculosis in Mice." Infection and Immunity 69, no. 12 (December 1, 2001): 7711–17. http://dx.doi.org/10.1128/iai.69.12.7711-7717.2001.

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ABSTRACT Murine macrophages effect potent antimycobacterial function via the production of nitric oxide by the inducible isoform of the enzyme nitric oxide synthase (NOS2). The protective role of reactive nitrogen intermediates (RNI) against Mycobacterium tuberculosisinfection has been well established in various murine experimental tuberculosis models using laboratory strains of the tubercle bacillus to establish infection by the intravenous route. However, important questions remain about the in vivo importance of RNI in host defense against M. tuberculosis. There is some evidence that RNI play a lesser role following aerogenic, rather than intravenous,M. tuberculosis infection of mice. Furthermore, in vitro studies have demonstrated that different strains of M. tuberculosis, including clinical isolates, vary widely in their susceptibility to the antimycobacterial effects of RNI. Thus, we sought to test rigorously the protective role of RNI against infection with recent clinical isolates of M. tuberculosis following both aerogenic and intravenous challenges. Three recently isolated and unique M. tuberculosis strains were used to infect both wild-type (wt) C57BL/6 and NOS2 gene-disrupted mice. Regardless of the route of infection, NOS2−/− mice were much more susceptible than wt mice to any of the clinical isolates or to either the Erdman or H37Rv laboratory strain of M. tuberculosis. Mycobacteria replicated to much higher levels in the organs of NOS2−/− mice than in those of wt mice. Although the clinical isolates all exhibited enhanced virulence in NOS2−/− mice, they displayed distinct growth rates in vivo. The present study has provided results indicating that RNI are required for the control of murine tuberculous infection caused by both laboratory and clinical strains of M. tuberculosis. This protective role of RNI is essential for the control of infection established by either intravenous or aerogenic challenge.

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Rakotosamimanana, Niaina, Vaomalala Raharimanga, Soa Fy Andriamandimby, Jean-Louis Soares, T. Mark Doherty, Maherisoa Ratsitorahina, Herimanana Ramarokoto, et al. "Variation in Gamma Interferon Responses to Different Infecting Strains of Mycobacterium tuberculosis in Acid-Fast Bacillus Smear-Positive Patients and Household Contacts in Antananarivo, Madagascar." Clinical and Vaccine Immunology 17, no. 7 (May 12, 2010): 1094–103. http://dx.doi.org/10.1128/cvi.00049-10.

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ABSTRACT The majority of healthy individuals exposed to Mycobacterium tuberculosis will not develop tuberculosis (TB), though many may become latently infected. More precise measurement of the human immune response to M. tuberculosis infection may help us understand this difference and potentially identify those subjects most at risk of developing active disease. Gamma interferon (IFN-γ) production has been widely used as a proxy marker to study infection and to examine the human immune response to specific M. tuberculosis antigens. It has been suggested that genetically distinct M. tuberculosis strains may invoke different immune responses, although how these differences influence the immune responses and clinical outcome in human tuberculosis is still poorly understood. We therefore evaluated the antigen-specific IFN-γ production responses in peripheral blood mononuclear cells from two cohorts of subjects recruited in Antananarivo, Madagascar, from 2004 to 2006 and examined the influence of the infecting M. tuberculosis strains on this response. The cohorts were sputum-positive index cases and their household contacts. Clinical strains isolated from the TB patients were typed by spoligotyping. Comparison of the IFN-γ responses with the spoligotype of the infecting clinical strains showed that “modern” M. tuberculosis strains, like Beijing and Central Asian (CAS) strains, tended to induce lower IFN-γ responses than “ancient” strains, like East African-Indian (EAI) strains, in index cases and their household contacts. These results suggest that new strains may have evolved to induce a host response different from that of ancient strains. These findings could have important implications in the development of therapeutic and diagnostic strategies.

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Journal articles on the topic 'M. tuberculosis Infection'

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