Relevant bibliographies by topics / Murine Mycobacterium tuberculosis infection

Academic literature on the topic 'Murine Mycobacterium tuberculosis infection'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Murine Mycobacterium tuberculosis infection"

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Juffermans, Nicole P., Jaklien C. Leemans, Sandrine Florquin, Annelies Verbon, Arend H. Kolk, Peter Speelman, Sander J. H. van Deventer, and Tom van der Poll. "CpG Oligodeoxynucleotides Enhance Host Defense during Murine Tuberculosis." Infection and Immunity 70, no. 1 (January 2002): 147–52. http://dx.doi.org/10.1128/iai.70.1.147-152.2002.

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ABSTRACT Oligodeoxynucleotides (ODNs) containing unmethylated CpG motifs activate immune cells to produce cytokines. CpG ODNs protect mice against infections with intracellular bacteria by the induction of a T helper 1 (Th1) response. To determine the effect of CpG ODNs in pulmonary tuberculosis, mice were treated with CpG ODNs or control ODNs at the time of intranasal infection. CpG ODNs reduced mycobacterial outgrowth for up to 5 weeks after Mycobacterium tuberculosis infection and were associated with a decrease in inflammation in lung tissue. CpG treatment was also associated with elevated levels of gamma interferon (IFN-γ) and decreased levels of interleukin 4 in the lungs and an increased capacity of splenocytes to secrete Th1-type cytokines. CpG ODNs given 2 weeks after infection were still able to reduce mycobacterial outgrowth and to enhance a Th1 response 5 weeks postinfection. Administration of CpG ODNs to IFN-γ-gene-deficient mice failed to reduce mycobacterial outgrowth. These data suggest that CpG ODNs improve host defense during pulmonary tuberculosis by an IFN-γ-dependent mechanism.
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Gilpin, Trey E. "Migration Kinetics and Migratory Morphology of Mycobacterium-Infected CD11c-eYFP Murine Bone Marrow Derived Cells." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 102.12. http://dx.doi.org/10.4049/jimmunol.200.supp.102.12.

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Abstract Central nervous system tuberculosis (CNSTB) is the most serious manifestation of extrapulmonary tuberculosis infections that represent 5–10% of all cases. Although migration of mycobacterium infected cells from the lung to the CNS is critical in bacterial dissemination into the CNS, very little is known about the migratory phenotypic changes of mycobacterium infected cells and overall the mechanism of dissemination into the brain is poorly understood. Mycobacterium tuberculosis is an obligate pathogenic bacterial species with it’s only mode of transportation being within innate immune cells. Dendritic cells (DCs) are potent antigen presenting cells that migrate long distances and through interactions with T-cells, initiate the adaptive immune response. Our lab has previously shown DCs are able to leave Mycobacterial granulomatous lesions from the lung with bacteria intact. Here we used live cell imaging of an under-agarose migration assay and cell tracking to define the kinetics of CD11c-eYFP DC migration during Mycobacterial infection. We found that migration of mycobacterium infected cells was impaired towards CCL19 chemokine and infected cells portrayed a migratory morphology distinct from uninfected DCs. With the use of CD11c-eYFP-LifeAct-RFP reporter mice, we characterized actin polymerization dynamics within infected CD11c cells. As actin polymerization plays a central role in cell migration, morphology, and pathogen internalization, to understand this process during mycobacterial infection will lead to novel therapeutic therapies to modulate dissemination into the CNS.
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Saviola, Beatrice, Samuel C. Woolwine, and William R. Bishai. "Isolation of Acid-Inducible Genes of Mycobacterium tuberculosis with the Use of Recombinase-Based In Vivo Expression Technology." Infection and Immunity 71, no. 3 (March 2003): 1379–88. http://dx.doi.org/10.1128/iai.71.3.1379-1388.2003.

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ABSTRACT A better understanding of mycobacterial gene regulation under certain stress conditions (e.g., low pH) may provide insight into mechanisms of adaptation during infection. To identify mycobacterial promoters induced at low pH, we adapted the recombinase-based in vivo expression technology (RIVET) promoter trap system for use with mycobacteria. Our results show that the TnpR recombinase of transposon γδ is active in Mycobacterium smegmatis and Mycobacterium tuberculosis. We developed a method to perform sequential double selection with mycobacteria by using RIVET, with a kanamycin preselection and a sucrose postselection. A library of M. tuberculosis DNA inserted upstream of tnpR was created, and using the double selection, we identified two promoters which are upregulated at low pH. The promoter regions drive the expression of a gene encoding a putative lipase, lipF (Rv3487c), as well as a PE-PGRS gene, Rv0834c, in a pH-dependent manner in both M. smegmatis and M. tuberculosis. The acid inducibility of lipF and Rv0834c was independent of the stress response sigma factor, SigF, as acid induction of the two genes in an M. tuberculosis sigF mutant strain was similar to that in the wild-type strain. No induction of lipF or Rv0834c was observed during infection of J774 murine macrophages, an observation which is in agreement with previous reports on the failure of phagosomes containing M. tuberculosis to acidify.
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Quiding-Järbrink, Marianne, Debbie A. Smith, and Gregory J. Bancroft. "Production of Matrix Metalloproteinases in Response to Mycobacterial Infection." Infection and Immunity 69, no. 9 (September 1, 2001): 5661–70. http://dx.doi.org/10.1128/iai.69.9.5661-5670.2001.

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ABSTRACT Matrix metalloproteinases (MMPs) constitute a large family of enzymes with specificity for the various proteins of the extracellular matrix which are implicated in tissue remodeling processes and chronic inflammatory conditions. To investigate the role of MMPs in immunity to mycobacterial infections, we incubated murine peritoneal macrophages with viable Mycobacterium bovis BCG or Mycobacterium tuberculosis H37Rv and assayed MMP activity in the supernatants by zymography. Resting macrophages secreted only small amounts of MMP-9 (gelatinase B), but secretion increased dramatically in a dose-dependent manner in response to either BCG or M. tuberculosis in vitro. Incubation with mycobacteria also induced increased MMP-2 (gelatinase A) activity. Neutralization of tumor necrosis alpha (TNF-α), and to a lesser extent interleukin 18 (IL-18), substantially reduced MMP production in response to mycobacteria. Exogenous addition of TNF-α or IL-18 induced macrophages to express MMPs, even in the absence of bacteria. The immunoregulatory cytokines gamma interferon (IFN-γ), IL-4, and IL-10 all suppressed BCG-induced MMP production, but through different mechanisms. IFN-γ treatment increased macrophage secretion of TNF-α but still reduced their MMP activity. Conversely, IL-4 and IL-10 seemed to act by reducing the amount of TNF-α available to the macrophages. Finally, infection of BALB/c or severe combined immunodeficiency (SCID) mice with either BCG or M. tuberculosis induced substantial increases in MMP-9 activity in infected tissues. In conclusion, we show that mycobacterial infection induces MMP-9 activity both in vitro and in vivo and that this is regulated by TNF-α, IL-18, and IFN-γ. These findings indicate a possible contribution of MMPs to tissue remodeling processes that occur in mycobacterial infections.
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Stokes, R. W., and D. P. Speert. "Lipoarabinomannan inhibits nonopsonic binding of Mycobacterium tuberculosis to murine macrophages." Journal of Immunology 155, no. 3 (August 1, 1995): 1361–69. http://dx.doi.org/10.4049/jimmunol.155.3.1361.

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Abstract The initial phagocytic interaction between Mycobacterium tuberculosis and macrophages (M phi) in the lung is probably nonopsonic, which would mean that M phi receptors will bind directly to bacterial ligands without the involvement of serum opsonins. Lipoarabinomannan (LAM) is a major component of the cell wall of mycobacteria. The possibility that LAM is involved in the nonopsonic binding of M. tuberculosis to M phi was investigated by using competitive inhibition assays. LAM inhibited binding of M. tuberculosis to murine peritoneal M phi in a dose-dependent manner. LAM also inhibited the binding of Mycobacterium avium and Mycobacterium bovis BCG to M phi. Phosphatidylinositol mannoside and lipomannan have the same phosphatidylinositol (PI) moiety as LAM, but differ in their glycosylation patterns. Both molecules inhibited binding of M. tuberculosis to M phi. Deacylation of LAM abrogated its capacity to inhibit binding of M. tuberculosis to M phi. These observations indicated that it was the PI moiety of LAM that was important in mediating its inhibitory properties. In support of this hypothesis, commercial PI was shown to inhibit the binding of M. tuberculosis to M phi. Our results suggest that cellfree LAM is able to inhibit the binding of mycobacteria to M phi, but that it does not do so by competing with any interaction between M phi receptors and cell-associated LAM, because the PI end of the molecule is believed to be anchored in the bacterial plasma membrane, and therefore not available as a ligand on the cell surface. However, LAM that is released from M. tuberculosis in the course of its active replication during infection may be able to interfere with the phagocytic clearance of mycobacteria.
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Snewin, Valerie A., Marie-Pierre Gares, Peadar ÓGaora, Zahra Hasan, Ivor N. Brown, and Douglas B. Young. "Assessment of Immunity to Mycobacterial Infection with Luciferase Reporter Constructs." Infection and Immunity 67, no. 9 (September 1, 1999): 4586–93. http://dx.doi.org/10.1128/iai.67.9.4586-4593.1999.

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ABSTRACT Protective immunity to mycobacterial infection is incompletely understood but probably involves the coordinated interaction of multiple cell types and cytokines. With the aim of developing assays that might provide a surrogate measure of protective immunity, we have investigated the use of recombinant mycobacteria carrying luciferase reporter enzymes to assess the effectiveness of antimycobacterial immunity in model systems. Measurement of luminescence was shown to provide a rapid and simple alternative to the counting of CFU as a means of monitoring mycobacterial viability. We describe optimization of a luciferase reporter strain of Mycobacterium tuberculosis and demonstrate its application for the study of mycobacterial interactions with host cells in tissue culture and the rapid assessment of vaccine efficacy in a murine model.
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Linnemann, Lara C., Ulrich E. Schaible, and Tobias K. Dallenga. "Evaluation of Myeloperoxidase as Target for Host-Directed Therapy in Tuberculosis In Vivo." International Journal of Molecular Sciences 23, no. 5 (February 25, 2022): 2554. http://dx.doi.org/10.3390/ijms23052554.

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Due to the rise of tuberculosis cases infected with multi and extensively drug-resistant Mycobacterium tuberculosis strains and the emergence of isolates resistant to antibiotics newly in clinical use, host-directed therapies targeting pathogenesis-associated immune pathways adjunct to antibiotics may ameliorate disease and bacterial clearance. Active tuberculosis is characterized by neutrophil-mediated lung pathology and tissue destruction. Previously, we showed that preventing M. tuberculosis induced necrosis in human neutrophils by inhibition of myeloperoxidase (MPO) promoted default apoptosis and subsequent control of mycobacteria by macrophages taking up the mycobacteria-infected neutrophils. To translate our findings in an in vivo model, we tested the MPO inhibitor 4-aminobenzoic acid hydrazide (ABAH) in C3HeB/FeJ mice, which are highly susceptible to M. tuberculosis infection manifesting in neutrophil-associated necrotic granulomas. MPO inhibition alone or as co-treatment with isoniazid, a first-line antibiotic in tuberculosis treatment, did not result in reduced bacterial burden, improved pathology, or altered infiltrating immune cell compositions. MPO inhibition failed to prevent M. tuberculosis induced neutrophil necrosis in C3Heb/FeJ mice in vivo as well as in murine neutrophils in vitro. In contrast to human neutrophils, murine neutrophils do not respond to M. tuberculosis infection in an MPO-dependent manner. Thus, the murine C3HeB/FeJ model does not fully resemble the pathomechanisms in active human tuberculosis. Consequently, murine infection models of tuberculosis are not necessarily adequate to evaluate host-directed therapies targeting neutrophils in vivo.
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Randall, Philippa J., Nai-Jen Hsu, Dirk Lang, Susan Cooper, Boipelo Sebesho, Nasiema Allie, Roanne Keeton, et al. "Neurons Are Host Cells for Mycobacterium tuberculosis." Infection and Immunity 82, no. 5 (February 24, 2014): 1880–90. http://dx.doi.org/10.1128/iai.00474-13.

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ABSTRACTMycobacterium tuberculosisinfection of the central nervous system is thought to be initiated once the bacilli have breached the blood brain barrier and are phagocytosed, primarily by microglial cells. In this study, the interactions ofM. tuberculosiswith neuronsin vitroandin vivowere investigated. The data obtained demonstrate that neurons can act as host cells forM. tuberculosis.M. tuberculosisbacilli were internalized by murine neuronal cultured cells in a time-dependent manner after exposure, with superior uptake by HT22 cells compared to Neuro-2a cells (17.7% versus 9.8%). Internalization ofM. tuberculosisbacilli by human SK-N-SH cultured neurons suggested the clinical relevance of the findings. Moreover, primary murine hippocampus-derived neuronal cultures could similarly internalizeM. tuberculosis. InternalizedM. tuberculosisbacilli represented a productive infection with retention of bacterial viability and replicative potential, increasing 2- to 4-fold within 48 h.M. tuberculosisbacillus infection of neurons was confirmedin vivoin the brains of C57BL/6 mice after intracerebral challenge. This study, therefore, demonstrates neurons as potential new target cells forM. tuberculosiswithin the central nervous system.
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Manabe, Yukari C., Cherise P. Scott, and William R. Bishai. "Naturally Attenuated, Orally Administered Mycobacterium microti as a Tuberculosis Vaccine Is Better than Subcutaneous Mycobacterium bovis BCG." Infection and Immunity 70, no. 3 (March 2002): 1566–70. http://dx.doi.org/10.1128/iai.70.3.1566-1570.2002.

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ABSTRACT Mycobacterium microti is phylogenetically closely related to Mycobacterium tuberculosis and is a member of that complex of organisms. It is a curved, acid-fast bacillus that is naturally attenuated with a narrow host range for Microtus species only. In this study, we confirm the unique susceptibility of voles to infection with M. microti and the relative resistance of mice with a significantly lower organism burden after 8 weeks of infection. In addition, histopathologic examination of lungs reveals a lack of cellular, granulomatous aggregates characteristically seen in murine M. tuberculosis infection. In the past, M. microti has been used successfully in humans as a vaccine against tuberculosis but was associated with cutaneous reactions. In an attempt to circumvent this adverse effect, we report the efficacy of aerosol and oral vaccination with M. microti. High-dose orogastric vaccination with M. microti resulted in a statistically significant improvement in protection against aerosol challenge with virulent M. tuberculosis in the murine model compared with subcutaneous M. bovis BCG Pasteur vaccination.
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Moreira, Andre L., Liana Tsenova, Melles Haile Aman, Linda-Gail Bekker, Sherry Freeman, Bande Mangaliso, Ulf Schröder, et al. "Mycobacterial Antigens Exacerbate Disease Manifestations in Mycobacterium tuberculosis-Infected Mice." Infection and Immunity 70, no. 4 (April 2002): 2100–2107. http://dx.doi.org/10.1128/iai.70.4.2100-2107.2002.

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ABSTRACT To control tuberculosis worldwide, the burden of adult pulmonary disease must be reduced. Although widely used, Mycobacterium bovis BCG vaccination given at birth does not protect against adult pulmonary disease. Therefore, postexposure vaccination of adults with mycobacterial antigens is being considered. We examined the effect of various mycobacterial antigens on mice with prior M. tuberculosis infection. Subcutaneous administration of live or heat-treated BCG with or without lipid adjuvants to infected mice induced increased antigen-specific T-cell proliferation but did not reduce the bacterial load in the lungs and caused larger lung granulomas. Similarly, additional mycobacterial antigen delivered directly to the lungs by aerosol infection with viable M. tuberculosis mixed with heat-killed Mycobacterium tuberculosis (1:1) also did not reduce the bacillary load but caused increased expression of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), which was associated with larger granulomas in the lungs. When M. tuberculosis-infected mice were treated with recombinant BCG that secreted cytokines shown to reduce disease in a preinfection vaccine model, the BCG secreting TNF-α, and to a lesser extent, IL-2 and gamma interferon (IFN-γ), caused a significant increase in granuloma size in the lungs. Moreover, treatment of M. tuberculosis-infected mice with recombinant murine TNF-α resulted in increased inflammation in the lungs and accelerated mortality without affecting the bacillary load. Taken together, these studies suggest that administration of mycobacterial antigens to mice with prior M. tuberculosis infection leads to immune activation that may exacerbate lung pathology via TNF-α-induced inflammation without reducing the bacillary load.
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Dissertations / Theses on the topic "Murine Mycobacterium tuberculosis infection"

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Bouzid, Feriel. "La Canettose, une maladie infectieuse émergente dans la corne de l'Afrique." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0548/document.

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La tuberculose est l’une des maladies infectieuses mortelles les plus fréquentes, causée par des mycobactéries tuberculeuses dont principalement M. tuberculosis. Notre thèse a porté sur Mycobacterium canettii caractérisée par un morphotype lisse et un temps de génération plus court que M. tuberculosis. Notre revue de la littérature a montré que moins d'une centaine de cas d’infection à M. canettii ont été rapportés majoritairement à Djibouti située dans la Corne de l’Afrique. Ensuite, notre étude prospective de la tuberculose pulmonaire à Djibouti a mesuré une prévalence d’infections à M. canettii de 4%. A travers un modèle murin d’infection par gavage, nous avons observé la translocation de M. canettii des intestins vers la circulation lymphatique et sanguine ; suivie par une dissémination principalement vers les poumons et les ganglions lymphatiques. Cette étude a alors démontré que M. canettii peut infecter les individus par voie orale et a révélé que M. canettii peut interagir avec le tissu adipeux brun. Ensuite, à travers des modèles cellulaires d’infection, nous avons montré que les pré-adipocytes bruns pourraient constituer une cible potentielle des mycobactéries tuberculeuses et que M. canettii ne persiste pas dans les adipocytes matures contrairement à M. tuberculosis. En conclusion, nous avons apporté des connaissances nouvelles sur l’infection à M. canettii : sa prévalence, son mode de transmission ainsi que de nouvelles pistes sur de possibles réservoirs environnementaux. L’ensemble de ces données suggèrent que l’infection à M. canettii doit être considérée comme une entité clinique distincte de la tuberculose que nous proposons de nommer « Canettose »
Tuberculosis is one of the most frequent deadly infectious diseases worldwide, caused by tuberculous mycobacteria including mainly M. tuberculosis. Our thesis focused on Mycobacterium canettii characterized by a smooth morphotype and a shorter generation time than M. tuberculosis. Our review of the literature showed that less than one hundred cases of M. canettii infection have been reported in Djibouti situated in the Horn of Africa. Then, our prospective microbiological study of pulmonary tuberculosis in Djibouti measured a prevalence of M. canettii lung infections of 4%. Through a mouse model by gavage, we observed the translocation of M. canettii from the intestines to the lymphatic and blood circulation; followed by dissemination mainly to the lungs and lymph nodes. In conclusion, this study demonstrated that M. canettii can follow the digestive tract to infect individuals and revealed also that M. canettii can interact with brown adipose tissue. Then, through cell infection models, we have shown that brown pre-adipocytes may be a potential target for tuberculous mycobacteria and that M. does not persist in mature adipocytes contrary to M. tuberculosis. In conclusion, this work allowed to bring new knowledge about M. canettii infection: its prevalence, its mode of transmission as well as new avenues on possible environmental reservoirs. All of these data suggest that M. canettii infection should be considered as a distinct clinical entity from tuberculosis. We propose to name "Canettosis" the M. canettii infection
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Khor, Siew Yan. "The immunomodulating activity of levamisole and gamma-interferon on experimental murine infections with Mycobacterium microti and Mycobacterium tuberculosis and the influence of gamma-interferon on the bactericidal activity of Isoniazid and Rifampicin." Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37744.

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Gurcha, Sudagar Singh. "Mannan biosynthesis in mycobacterium tuberculosis." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324798.

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Barr, D. A. "Characterising HIV-associated Mycobacterium tuberculosis blood stream infection." Thesis, University of Liverpool, 2018. http://livrepository.liverpool.ac.uk/3028670/.

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Despite the success of antiretroviral therapy roll-out, one-million people still die with HIV-infection annually. In high-burden settings, tuberculosis remains the most common proximal cause of hospital admission and death in people living with HIV. In post-mortem series, 90% of fatal HIV-associated tuberculosis is 'disseminated'. This is a form of tuberculosis which has been poorly characterised and, despite the high associated-mortality, never been the subject of interventional trials to define optimal treatment strategies. This thesis contends that the mode of severe HIV-associated tuberculosis is blood stream infection. First it is argued with reference to historical literature that blood stream dissemination is part of the natural history of post-primary tuberculosis infection, and that HIV-associated M. tuberculosis blood stream infection (MTBBSI) can be conceived of as a reversion to, and exaggerated form of this natural history. Using data from a large cohort (n=571) of HIV-infected inpatients with CD4 cell count < 350 cells/mm3 and a new TB diagnosis from Khayelitsha Hospital, South Africa (the KDHTB study), the extent and magnitude of MTBBSI is shown to be a major determinant of clinical phenotype and mortality risk. Systematic, quantitative markers of blood stream dissemination, including TB blood culture, urine-lipoarabinomannan (uLAM), and urine GeneXpert MTB/RIF testing (uXpert), can be combined into a 'disseminated TB score. KDHTB patients have high prevalence of abnormal sodium and fluid balance, metabolic acidosis associated with acute kidney injury, hyperlactataemia, infiltrative liver and splenic pathology, and anaemia. Each of these pathophysiologies in turn correlates to disseminated TB score, and to risk of death, suggesting bacterial burden and MTBBSI are central to the pathophysiology of severe HIV-associated tuberculosis. An individual patient data meta-analysis, with 20 independent data sets comprising over 6000 patients, is used to establish the prevalence of TB blood culture positive disease amongst critically unwell HIV-infected inpatients. This shows that MTBBSI is more common than previous estimates suggest, is a strong independent association with mortality risk, and is also associated with specific increased risk of death if empirical treatment is delayed. The development of tools to identify and measure MTBBSI is described, including Xpert-ultra testing of blood, and the use of a novel dye, DMN-trehalose, to perform direct microscopy on patient blood samples. These techniques are used to provide the first description of the pharmacodynamics of MTBBSI, by serially quantifying blood bacilli load over the first 72-hours of standard TB therapy, in 28 patients with high predicted probability of bacteraemia. In this cohort, risk of mortality is related to several summary measures of MTBBSI dynamics in the first 72-hours of therapy, suggesting this approach can be used to define biomarkers of treatment response. In conclusion, MTBBSI is a highly-specific diagnosis responsible for substantial mortality in hospitalised people living with HIV. Interventions with strengthened bacteriocidal activity, focussed on reducing bacterial burden, are warranted for MTBBSI. Tools developed in this thesis, including potential pharmacodynamic biomarkers, should facilitate such trials.
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Mitchell, Joni. "Reinfection dynamics of mycobacterium tuberculosis." Thesis, Cape Peninsula University of Technology, 2007. http://hdl.handle.net/20.500.11838/1474.

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Thesis (MTech (Biomedical Technology))--Cape Peninsula University of Technology, 2007
Reinfection is an important mechanism leading to recurrent tuberculosis. Recently, molecular epidemiological studies have shown that in high incidence settings, recurrent tuberculosis may occur through reinfection. Animal model experiments have shown that a reinfecting mycobacterial strain is specifically targeted to existing granulomas and that these structures are more dynamic than was previously thought. In this study we hypothesised that primary infection with M. tuberculosis may reprogramme human macrophages thereby preventing or facilitating reinfection with a secondary mycobacterial strain. Two antibiotic-resistant M. tuberculosis H37Rv variants were generated by electrotransformation of marked plasmids, designated KanRand HygR . A THP1 human macrophage cell line was infected and reinfected with different combinations of these marked strains as well as a hypervirulent M. tuberculosis Beijing strain. Mycobacterial growth has been assessed by colony forming unit enumeration and confirmed with polymerase chain reaction (PCR) analysis. In vitro growth curves of wild-type and differentially marked M. tuberculosis H37Rv Kan Rand HygR strains were compared in the BACTECTM mycobacterial growth indicator tube (MGITTM) system in parallel with conventional liquid culturing. In vitro liquid culture growth curves of hypervirulent clinical Beijing strain isolates were also compared to M. tuberculosis H37Rv growth curves. Through this it was established that there was no fitness cost as result of plasmid integration and that these strains of varying virulence had similar growth curves. Competitive dynamics within THP1 human macrophage cells were then assessed and have shown that there were no significant differences in growth patterns between primary and secondary infecting strains during THP1 cell reinfection. The findings of this study answered fundamental questions regarding reinfection of mycobacterial strains. It was established here that human macrophages can indeed be reinfected with a second virulent mycobacterial strain.
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Alexi, Nancy. "Interactions of Mycobacterium tuberculosis strain H37Rv with murine peritoneal macrophages." Thesis, University of Reading, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292725.

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Krüüner, Annika. "Drug-resistant Mycobacterium tuberculosis in Estonia /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-455-0/.

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Hamerman, Jessica Ann. "Macrophage activation during Mycobacterium bovis BCG infection /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8359.

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Millington, Kerry. "Functional antigen-specific T cell responses to Mycobacterium tuberculosis infection." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437349.

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Estorninho, Megan. "Studies on mycobacterium tuberculosis transcriptional regulators involved in intracellular infection." Thesis, University of Surrey, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511105.

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Books on the topic "Murine Mycobacterium tuberculosis infection"

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O, Thoen Charles, and Steele James H, eds. Mycobacterium bovis infection in animals and humans. Ames, Iowa: Iowa State University Press, 1995.

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O, Thoen Charles, Steele James H, and Gilsdorf Michael J, eds. Mycobacterium bovis infection in animals and humans. 2nd ed. Ames, Iowa: Blackwell Pub., 2006.

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Venketaraman, Vishwanath, ed. Understanding the Host Immune Response Against Mycobacterium tuberculosis Infection. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97367-8.

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Hasnain, Seyed Ehtesham, Nasreen Z. Ehtesham, and Sonam Grover, eds. Mycobacterium Tuberculosis: Molecular Infection Biology, Pathogenesis, Diagnostics and New Interventions. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9413-4.

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Hingley-Wilson, Suzanne Maria. The detection and identification of macrophage genes induced by intracellular infection with mycobacterium tuberculosis. Birmingham: University of Birmingham, 1998.

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Alli, Oyebode Armstrong Terry. Development of a RAP-PCR strategy to study mycobacterium tuberculosis gene expression during intracellular infection of macrophages. Birmingham: University of Birmingham, 1998.

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Steele, James H., Charles O. Thoen, and Michael J. Gilsdorf. Mycobacterium Bovis Infection in Animals and Humans. Wiley & Sons, Incorporated, John, 2008.

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Understanding the Host Immune Response Against Mycobacterium tuberculosis Infection. Springer, 2018.

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Understanding the Host Immune Response Against Mycobacterium tuberculosis Infection. Springer, 2018.

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Steele, James H., Charles O. Thoen, and Michael J. Gilsdorf. Mycobacterium Bovis Infection in Animals and Humans. Wiley & Sons, Incorporated, John, 2010.

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Book chapters on the topic "Murine Mycobacterium tuberculosis infection"

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Lienard, Julia, and Fredric Carlsson. "Murine Mycobacterium marinum Infection as a Model for Tuberculosis." In Methods in Molecular Biology, 301–15. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6673-8_20.

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Harris, James, Sergio De Haro, and Vojo Deretic. "Autophagy and Mycobacterium tuberculosis." In Autophagy in Immunity and Infection, 127–38. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/352760880x.ch6.

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Chiang, Chen-Yuan, Sven Gudmund Hinderaker, Hsien-Ho Lin, and Donald A. Enarson. "Latent Infection with Mycobacterium tuberculosis." In Handbook of Global Tuberculosis Control, 359–68. Boston, MA: Springer US, 2017. http://dx.doi.org/10.1007/978-1-4939-6667-7_21.

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Kolloli, Afsal, Pooja Singh, and Selvakumar Subbian. "Granulomatous Response to Mycobacterium tuberculosis Infection." In Understanding the Host Immune Response Against Mycobacterium tuberculosis Infection, 41–66. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97367-8_3.

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Johnson, Benjamin K., Sean M. Thomas, Andrew J. Olive, and Robert B. Abramovitch. "Macrophage Infection Models for Mycobacterium tuberculosis." In Methods in Molecular Biology, 167–82. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1460-0_6.

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Johnson, Benjamin K., and Robert B. Abramovitch. "Macrophage Infection Models for Mycobacterium tuberculosis." In Methods in Molecular Biology, 329–41. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2450-9_20.

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Domingo-Gonzalez, Racquel, Oliver Prince, Andrea Cooper, and Shabaana A. Khader. "Cytokines and Chemokines in Mycobacterium tuberculosis Infection." In Tuberculosis and the Tubercle Bacillus, 33–72. Washington, DC, USA: ASM Press, 2017. http://dx.doi.org/10.1128/9781555819569.ch2.

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Toossi, Zahra. "The Inflammatory Response in Mycobacterium Tuberculosis Infection." In Inflammation, 139–51. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9702-9_11.

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Hanna, Luke Elizabeth. "Coinfection with Mycobacterium tuberculosis and HIV." In Understanding the Host Immune Response Against Mycobacterium tuberculosis Infection, 127–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97367-8_7.

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Sharma, Surendra K., and Alladi Mohan. "Extrapulmonary Tuberculosis." In Mycobacterium Tuberculosis: Molecular Infection Biology, Pathogenesis, Diagnostics and New Interventions, 37–53. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9413-4_4.

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Conference papers on the topic "Murine Mycobacterium tuberculosis infection"

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Pasula, Rajamouli, and Francis X. McCormack. "Keratinocyte Growth Factor Attenuates Murine Pulmonary Mycobacterium Tuberculosis Infection Through GM-CSF Dependent Mechanisms." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3335.

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Schweisfurth, H., U. Hinzen, and D. Specht. "Mycobacterium Tuberculosis Infection in Patients with Various Respiratory Diseases." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4781.

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Bussi, C., M. Silva Dos Santos, E. M. Bernard, P. Santucci, J. I. Macrae, and M. G. Gutierrez. "The metabolic response of human macrophages to Mycobacterium tuberculosis infection." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.65.

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Adewole, Olanisun Olufemi, O. Kayode, O. Abe, Harriet Osunkoya, Babatope Kolawole, Rosemary Ikem, Tayo Adewole, and Greg Erhabor. "Latent mycobacterium tuberculosis infection among type 2 diabetes mellitus patients." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2979.

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Coleman, Michelle M., Stephen H. MacDonald, Elliott Woodward, Emma R. Dorris, Parthiban Nadarajan, Wui-Mei Chew, Anne-Marie McLaughlin, and Joseph M. Keane. "Networked T Cell Death Following Macrophage Infection By Mycobacterium Tuberculosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1016.

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Agrawal, N., D. Gekhman, E. S. Guy, and P. M. Alapat. "Non-Tuberculosis Mycobacterium Co-Infection Presenting as a Thoracic Mass." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3076.

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Kaminskiy, Grigory, Anna Panova, Vera Zimina, Alla Peregudova, Olga Kudrja, Elena Beloborodova, Olga Lovacheva, Anastasia Samoilova, and Irina Vasilyeva. "Clinical and laboratory features of Mycobacterium avium complex infection in comparison with infection, caused by Mycobacterium tuberculosis, in HIV-infected patients." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4640.

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Tavolara, Thomas E., Muhammad Khan Khalid Niazi, Gillian Beamer, and Metin N. Gurcan. "Identifying lung imaging biomarkers of BCG vaccination after infection with Mycobacterium tuberculosis." In Digital and Computational Pathology, edited by John E. Tomaszewski and Aaron D. Ward. SPIE, 2021. http://dx.doi.org/10.1117/12.2581945.

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van Rensburg, Ilana, and Andre Loxton. "Utility of mycobacterium tuberculosis Rv0081-specific host gene expression to distinguish latent infection from active tuberculosis disease." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2113.

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Ucar, Tamer, Dilek Karahoca, and Adem Karahoca. "Predicting the existence of mycobacterium tuberculosis infection by Bayesian Networks and Rough Sets." In 2010 15th National Biomedical Engineering Meeting (BIYOMUT 2010). IEEE, 2010. http://dx.doi.org/10.1109/biyomut.2010.5479850.

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You might also be interested in the extended bibliographies on the topic 'Murine Mycobacterium tuberculosis infection' for particular source types:
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