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Artykuły w czasopismach na temat "M. tuberculosis Infection"
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Small, P. M. "M tuberculosis and HIV infection". Biomedicine & Pharmacotherapy 47, nr 8 (styczeń 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 i David McDonald. "Mycobacterium tuberculosis Promotes HIV trans-Infection and Suppresses Major Histocompatibility Complex Class II Antigen Processing by Dendritic Cells". Journal of Virology 84, nr 17 (30.06.2010): 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 i 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, nr 2 (1.03.2005): 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 i O. V. Stopolyanskyi. "A modern view on the mechanism of occurrence and development of latent tuberculosis infection. Literature review". Tuberculosis, Lung Diseases, HIV Infection, nr 3 (27.09.2022): 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 i 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, nr 01 (marzec 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 i Issar Smith. "Global Transcriptional Profile of Mycobacterium tuberculosis during THP-1 Human Macrophage Infection". Infection and Immunity 76, nr 2 (10.12.2007): 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 i 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, nr 3 (28.11.2021): 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 i Eduardo Sada. "Human β-Defensin 2 Is Expressed and Associated with Mycobacterium tuberculosis during Infection of Human Alveolar Epithelial Cells". Infection and Immunity 73, nr 8 (sierpień 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 i Rohinton Mulla. "Determination of Urinary Neopterin/Creatinine Ratio to Distinguish Active Tuberculosis from Latent Mycobacterium tuberculosis Infection". Journal of Biomarkers 2016 (28.06.2016): 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, i Fatmawati Fatmawati. "Peranan Sel Sistem Imun Alamiah Pada Infeksi Mycobacterium tuberculosis". Jurnal Ilmu Kedokteran (Journal of Medical Science) 16, nr 2 (20.10.2022): 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.
Rozprawy doktorskie na temat "M. tuberculosis Infection"
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Du, Toit Eben Francois. "Modelling the co-infection dynamics of HIV-1 and M. tuberculosis". Diss., Pretoria : [s.n.], 2008. http://upetd.up.ac.za/thesis/available/etd-08172008-213855.
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Chiacchiaretta, Matteo. "M. tuberculosis lineages: genetic diversity and its involvement on macrophage infection and on drug tolerance". Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1183830.
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A central feature of Mycobacterium tuberculosis pathogenesis is the ability to survive within macrophages and colonize hostile environments that are acidic and rich in cholesterol and fatty acids.
The genetic variability among clinical isolates may have dramatic consequences on the outcome of infections. Many in vitro and in vivo studies have demonstrated strain-dependent variation in key aspects of virulence such as stress survival, transmission, pathology, and lethality.
This variability in MTB clinical isolates went neglected for decades; however, recently the scientific community recognized it causes important consequences on the progression of infection. As reduced host response is supposed to be the key to enabling MTB persistence and transmissibility, the immunological state of the host is also important to consider when studying the relative virulence of clinical MTB strains. In this context, the polarization states of macrophages have a huge impact on their function. It affects how macrophages can react to external signals, changing gene expression, membrane composition, receptor exposure, and cytokines production.
In our work, we focused our attention on MTB diversity and its role in pathogenesis and drug resistance acquisition. We proposed a comprehensive approach for better understanding MTB virulence taking into consideration both human (phenotypic) and MTB (genetic) variability.
We selected well-characterized strains belonging to specific MTB lineages and adopt the THP-I-derived macrophage infection model, but considering host variability by deriving M1 or M2 polarized macrophages.
Confocal live microscopy was used to study at a single-cell level different macrophage pathways during the infection. These included phagolysosomal acidification, autophagic flux, and apoptosis. All are mechanisms that MTB hijacks in order to survive within the host. Cytokine profiles were measured in response to the different MTB lineages, along with the survival of both the macrophages and the bacteria at different time points post-infection.
In M1 macrophages, whereas less virulent/ancient are more efficient in blocking the phagosomal acidification, more virulent/modern strains are likely better at tolerating the acidic environment. However, the number of responsive macrophages remained relatively low. In M2a macrophages, whereas less virulent/ancient strains are less efficient in blocking the phagolysosomal acidification, more virulent/modern strains are blocking phagolysosomal acidification. The number of responsive macrophages was found to vary depending upon the features of the infecting strains, with the most virulent ones inducing the lowest percentages of acidifying cells.
The analysis of the autophagic flux showed less heterogeneity among both the bacterial strains and the macrophage phenotypes considered. Indeed, the induction of autophagy was found negligible in our observations.
In M1 macrophages, bystander non-infected cells of more virulent/ modern showed increased apoptosis (40%). Stratification of the data by mycobacterial burden showed similar apoptotic levels irrespective of the mycobacterial load, despite a trend displaying slightly higher apoptotic levels in bystander non-infected cells or in cells infected with a lower number of mycobacteria could be noted. In contrast, none of the categories induced apoptosis in M2 macrophages at the time point considered.
In M1 cells, the infection with less virulent/ancient lineages reduced the production of pro-inflammatory IL1-β. Likewise, IL-18 levels were lower in M1 cells infected with less virulent/ancient lineages. The chemokine GROα showed a similar pattern between MTB categories considered. In M2 cells we observed the modulation of anti-inflammatory IL-10 when comparing clinical to laboratory strains. Most of the statistically significant differences found were observed within 24h for both polarization types.
Our findings on macrophage survival corroborate the results obtained at the single-cell level, with more virulent/modern lineages causing increased cell death. Interestingly, these data seem to contrast the finding that such strains showed lower macrophage entry in colony-forming units evaluation studies. Similarly, there was not a direct correlation between pro-inflammatory cytokine production and macrophage killing. Nevertheless, more virulent/modern strains showed increased intramacrophagic replicative capacity compared to less virulent/ancient lineages.
We also studied the genetic variability of the MTB strains during drug resistance acquisition. Among newly investigated mechanisms, the role of smallRNAs in the development of drug resistance has been considered in other bacteria but remains unexplored in MTB. We characterized the smallRNA ncRv0842c, cis-encoded to the Rv0842 gene which codes for a putative efflux pump reported to be involved in rifampicin resistance (RIF-R) development. Accordingly, the present study characterized the role of ncRv0842c during RIF challenge and validated the role of a lineage-specific synonymous mutation on the coding region of Rv0842 affecting the promoter region of the cis-encoded smallRNA.
In order to understand the role of the smallRNA in modulating the efflux pump, we characterized its expression during challenge experiments using sub-inhibitory concentrations of rifampicin. We then generated overexpressing mutants from MTB-selected ancient and modern strains.
qPCR showed basal downregulation of ncRv0842 in ancient lineages compared to modern lineages. This result confirmed the hypothesis that the synonymous mutation in Rv0842 (L45L) specific for the ancient lineages, and abrogating the -10 promoter region of the antisense smallRNA is severely affecting the expression of the smallRNA. Under RIF-induced stress, we observed upregulation of Rv0842, and downregulation of the smallRNA only in H37Rv (modern lineage) whereas in L5 (ancient lineage) the smallRNA expression was not affected. MABA assay performed on modern lineage mutants overexpressing ncRv0842c showed a 1-dilution reduction of the MIC in comparison with their respective control (mock) while the ancient lineage strains did not show any MIC shift despite the overexpression of the smallRNA. Our analysis showed that the unraveling of smallRNA may provide new insights on MTB lineage-specific adaptation to drug-related stress and uncover the role of silent mutations in determining different phenotypes in MTB.
Our study can contribute to better understanding lineage-specific pathogenicity and highlights the importance of strain- and lineage-specific rational design and development of effective diagnostic tools and vaccines.
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Kieswetter, Nathan Scott. "Remodelling of Mycobacterial Peptidoglycan During Cell Division and the Epigenetics of Macrophages during M. tuberculosis infection". Doctoral thesis, Faculty of Health Sciences, 2021. http://hdl.handle.net/11427/33815.
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There are so many people who I would like to thank. If it takes a village to raise a child, it certainly takes a city to train a scientist. Firstly, I would like to thank my supervisors, A/Prof Reto Guler, Prof Frank Brombacher and Dr Mumin Ozturk for allowing me to further my studies and allowing me to work on several interesting projects. Specifically, I would like to take this opportunity to thank A/Prof Reto Guler for his insightful patient advice, training and ever willingness to talk about my work. His brilliant example has made me a better scientist. Further, I would also like to thank Dr Mumin Ozturk for his constant, patient mentorship, help, advice and friendship. His influence, guidance and example have affected me more than he'll ever know. Lastly, but certainly not least, I would like Professor Bavesh Kana and for all his advice and support. I would also like to express my gratitude to my labmates from the Brombacher group. All the conversations, laughs, celebrations and commiserations have made this journey undeniably easier. In particular, I would like to thank Shelby-Sara Jones for her constant willingness to help with lab work whilst chatting about everything under the sun. To my friends and family, there are no words to express my unending gratitude. Without their love and support along the way, I would never have gotten to this stage in my life. To my parents and sister, I would like to say a huge thank you for their constant support and love during my academic career so far. You guys have been wonderful. A huge thank you to Daniela de Almeida and the French's for their support and love from afar– you guys have been great. I would like to say a special thank you to Dustin Fischer who has always been there for a beer and good old-fashioned rant. I can only hope that my friendship and advice have been even the smallest bit as helpful to him as he has been to me during our long trek through academia. To the Cunniffes, thank you for all your support down this long road and truly making me feel like one of the family. Last but by no means least, I would like to thank my partner, Teagan Cunniffe, whose effortless grace, wit, humour, friendship and constant love have been the single greatest gifts I have ever received. I look forward to our adventures to come. Thank you for being there every step of the way and keeping me sane - This dissertation is dedicated to you.
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Roy, Eleanor. "Response of dendritic cells to Mycobacterium tuberculosis infection and the induction of protective immunity using dendritic cells infected with an auxotrophic mutant of M. tuberculosis". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446801/.
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Mycobacterium tuberculosis, the aetiological agent of tuberculosis, is an intracellular pathogen commonly infecting macrophages, and has also been shown to infect dendritic cells (DC). As DC are particularly effective antigen-presenting cells, it is likely that they play a principle role in initiating anti-mycobacterial T cell responses. This work investigates the activation of DC in response to M. tuberculosis infection using murine bone marrow-derived DCs, generated in the presence of granulocyte- macrophage colony-stimulating factor (GM-CSF). It was found that both unsorted DC populations and those sorted on CD11c+, were capable of supporting the survival and replication of wild type M. tuberculosis (H37Rv) in a manner similar to that observed in macrophages. Mycobacterial infection was found to be sufficient to activate the DC populations, particularly CD11c+ DC, to acquire a mature phenotype, as measured by cytokine production and expression of costimulatory and antigen presentation molecules on the cell surface. Further study showed that mycobacteria-infected DC could prime protective immunity in an experimental model of murine tuberculosis. This was carried out using a lysine auxotroph of M. tuberculosis. Infected DC were used to vaccinate syngeneic or allogeneic mice. Protection against challenge with wild type M. tuberculosis was observed in both cases, suggesting that recipient antigen-presenting cells crosspresented mycobacterial antigen from donor DC to induce a protective immune response. A similar protective response was observed on using a xenogeneic model, in which infected murine DC were used to vaccinate guinea pigs. Both CD4+ and CD8+ T cells harvested from spleens of vaccinated mice, showed specific production of interferon-y in response to mycobacterial antigen, indicating that crosspresentation by recipient antigen-presenting cells results in the effective priming of mycobacteria-specific T cells in vivo.
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Adankwah, Ernest [Verfasser]. "Pathognomonic effects of human tuberculosis on host immune response in an endemic population: impact on T-cell functions and M. tuberculosis infection diagnosis / Ernest Adankwah". Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1213094801/34.
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Neumann, Jan [Verfasser]. "Characterization of macrophage Frizzled1 expression and the role of Wnt3a-induced signaling in experimental M. tuberculosis infection / Jan Neumann". Lübeck : Zentrale Hochschulbibliothek Lübeck, 2010. http://d-nb.info/1004898347/34.
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Wyndham-Thomas, Chloe. "Screening for latent M. tuberculosis infection in HIV-positive patients residing in low tuberculosis incidence settings: Investigation of the current practices and identification of clinical- and immune-based strategies for improvement". Doctoral thesis, Universite Libre de Bruxelles, 2016. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/241270.
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Tuberculosis (TB) remains the main cause of death in people living with HIV (PLHIV). Indeed, PLHIV have a 20-30% greater risk of developing TB compared to HIV-uninfected subjects and have lower TB treatment success rates. In 2014, among the 9.6 million incident cases of TB reported worldwide, 12% occurred in PLHIV and 0.4 million deaths from HIV-associated TB were recorded.Mycobacterium tuberculosis is the main etiological agent for TB. For a majority of individuals, the immune response upon infection by M. tuberculosis is sufficient to prevent the development of disease, but insufficient to clear the bacteria. This leads to the persistence of viable M. tuberculosis in diverse cells with no resulting clinical manifestations, an entity known as latent tuberculosis infection (LTBI). The resulting reservoir of M. tuberculosis is vast, and an estimated one third of the world population is concerned. For subjects with LTBI, the life-time risk of reactivation and progression to TB lies between 5 and 10%. However, if co-infected with HIV, the risk is much greater and reaches 10% per year. According to a Cochrane review in 2010, the screening and treatment of LTBI in PLHIV reduces this risk by 30-60%. This prevention strategy is therefore widely recommended. However, the implementation of LTBI screening and treatment into standard HIV-care has been limited. In this work, three different approaches have been used to understand and address this issue, focusing on a low TB-incidence and high-income setting.The first approach was to assess the implementation of LTBI screening in HIV-care across Belgium and identify its barriers as perceived by the caregivers on the field. Raising awareness to this issue was an indirect objective of the study. A multi-choice questionnaire was sent to 55 physicians working in a Belgian AIDS reference center or satellite clinic. A response rate of 62% was obtained. Only 20% of participants performed LTBI screening on all their patients and notable variations in the screening methods used were observed. A large majority of participants were in favor of targeting LTBI screening to HIV-infected patients at highest risk of TB rather than a systematic screening of all PLHIV. These results have been communicated to the Belgian LTBI working group, currently updating the national LTBI screening guidelines. Indeed, targeting screening to those at highest risk of TB is an attractive strategy in low-TB incidence countries and is already recommended in the United Kingdom. However, to date, no score assessing the risk of TB in PLHIV has been validated. Among the barriers to LTBI screening identified by the participants of this first study, the most frequently reported were lack of sensitivity of screening tools, risk associated to polypharmacy and toxicity of treatment. Improving the sensitivity of LTBI screening was the cornerstone of the second approach. The available screening tools for LTBI are the tuberculin skin test (TST) and two Interferon-gamma release assays (IGRAs): the QuantiFERON-TB Gold-IT (QFT-GIT) and the T-SPOT.TB®. All three lack sensitivity in PLHIV. Various strategies to discover superior LTBI screening tools are therefore being explored, including the development of IGRAs in response to alternative M. tuberculosis antigens to those used in the QFT-GIT or T-SPOT.TB®. A potential candidate is the native Heparin-Binding Haemagglutin (nHBHA), a methylated M. tuberculosis protein regarded as a latency-associated antigen. An in-house IGRA based on nHBHA (nHBHA-IGRA) has been shown to be a promising LTBI screening tool both in immunocompetent adults and in hemodialysed patients. The contribution of this nHBHA-IGRA to the detection of M. tuberculosis in PLHIV was therefore investigated. Treatment-naïve HIV-infected subjects were recruited from 4 Brussels-based hospitals. Subjects underwent screening for latent TB using the nHBHA-IGRA in parallel to the classical method consisting of medical history, chest X-ray, TST and QFT-GIT. Prospective clinical and biological follow-up ensued, with repeated testing with nHBHA-IGRA. Among 48 candidates enrolled for screening, 9 were diagnosed with LTBI by combining the TST and QFT-GIT results (3 TST+/QFT-GIT+, 1 TST+/QFT-GIT- and 5 TST-/QFT-GIT+). All 3 TST+/QFT-GIT+ patients, the TST+/QFT-GIT- patient as well an additional 3 subjects screened positive with the nHBHA-IGRA. These 3 additional patients had known M. tuberculosis exposure risks compatible with LTBI. During follow-up (median 14 months) no case of TB was reported and nHBHA-IGRA results remained globally constant. Multiplex analysis confirmed IFN- as the best read-out for the assay. From this study, we concluded that the nHBHA-IGRA appears complementary to the QFT-GIT for the screening of LTBI in PLHIV and the combination of the two tests may increase the sensitivity of screening. A large-scale study is however necessary to determine whether combining nHBHA-IGRA and QFT-GIT offers sufficient sensitivity to dismiss TST, as suggested by our results. In the same study, a group of HIV-infected adults with clinical suspicion of active TB were also recruited and tested with nHBHA-IGRA. Contrary to results in HIV-uninfected subjects, the nHBHA-IGRA could not discriminate between LTBI and active TB in PLHIV. This is an important caveat as HIV-infected subjects may present subclinical TB.A different angle was used for the third approach to the problem of LTBI in PLHIV. Systemic immune activation (SIA) is one of the principal driving forces in the natural course of HIV-infection. Despite long-term viral suppression by combination antiretroviral treatment (cART), a low-level SIA persists and is associated with an early-onset of age-associated disorders such as cardiovascular disease, dementia and osteoporosis. Causes of SIA in PLHIV are multiple and certain chronic infections appear to be implicated. A recent study in South Africa found that LTBI in PLHIV was associated with an increase in circulating activated CD8+ T-cells. If LTBI should contribute to the persistence of SIA, its screening and treatment could have an additional benefit on the clinical outcome of PLHIV. To investigate this theory, the expression of T-cell activation markers (CD38 and HLADR) as well as the level of plasmatic markers of immune activation (IL-6, sCD14, D-Dimers) were compared between subjects presenting active TB, subjects with LTBI and M. tuberculosis-free persons, with and without HIV-infection. In accordance with previous studies, active TB was associated with higher levels of SIA biomarkers in both HIV-infected and -uninfected groups. Among the HIV-uninfected subjects, no significant difference in biomarker level was found between those presenting LTBI and those with no evidence of M. tuberculosis. The effect of LTBI on activation biomarkers in the HIV-infected groups remained inconclusive because of the small number of individuals in the HIV+/LTBI group. Further investigation is therefore warranted. Interestingly, it was found that plasmatic markers may have a greater sensitivity for the detection of M. tuberculosis-associated SIA than the T-cell activation markers, an important result for future studies.Overall, LTBI in PLHIV is a challenging topic, in particular because of the lack of a gold-standard for the diagnosis of LTBI. Despite suboptimal tools, the evident clinical impact of LTBI screening and treatment in PLHIV on TB incidence justifies its implementation in standard HIV-care. In low TB-incidence countries, who, when and how to screen for LTBI in PLHIV remains unclear. This work offers an overview on the subject with particular focus on possible measures for improvement in the field.Doctorat en Sciences médicales (Médecine)
info:eu-repo/semantics/nonPublished
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COLONE, ALESSIA. "Role of CpG ODNs in human macrophages before and after infection with Mycobacterium tuberculosis and their effects in cellular and molecular defence mechanisms". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1265.
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Oligodeoxynucleotides, containing unmethylated CpG dinucleotides within specific sequence contexts in bacterial or viral DNA, are detected as a danger signal by the vertebrate immune system. CpG motifs are sequences with a potent antymycobacterial activity and we tested a panel of eight synthetic CpG ODNs for their capacity to reduce Mycobacterium tuberculosis growth analyzing their effects in vitro in human macrophages. CpG2 ODN is able significantly to reduce pathogen growth while CpG3 ODN determines an enhancement in replication than control macrophages. In term of molecular and cellular mechanisms of defence in the host-pathogen interaction we found a specificity of CpG ODN sequence in intracellular pH decrease but not in Reactive Oxygen Species production, both influenced by CpG. Moreover we analyzed environment of macrophages, stimulated with these two CpG ODNs, before and after infection showing a correlation between mycobacterial growth and IFN- transcription following 1 hour of CpG treatment, and a down-regulation in IFN-mRNA upon pathogen contact. Finally we described a pathway of cytokines, among them SerpinE1 never associated before in M. tuberculosis infection involved in macrophages migration. In conclusion CpG ODNs could be used as vaccine adjuvants confirming their capacities
to improve protection against M. tuberculosis involving mechanisms of defence.
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Carmo, Ana Maria do. "Modulação da resposta imunológica no pulmão de Camundongos co-infectados com Mycobacterium bovis e Strongyloides venezuelensis". Universidade Federal de Juiz de Fora (UFJF), 2008. https://repositorio.ufjf.br/jspui/handle/ufjf/2989.
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Sabe-se que existem inúmeros trabalhos envolvendo a modulação da resposta imune ao Mycobacterium. No entanto, o número de indivíduos apresentando tuberculose é cada vez maior. A resposta imune ao Mycobacterium é desencadeada principalmente por linfócitos Th1, com a produção de IFN-γ. As parasitoses intestinais também representam um importante problema médico-sanitário, tendo em vista o grande número de pessoas acometidas e as inúmeras alterações orgânicas que podem provocar no hospedeiro. Essas infecções helmínticas induzem preferencialmente uma resposta Th2 com a produção de IL-4, IL-5 e IL-13. Este trabalho avaliou a regulação da resposta imune no pulmão de camundongos co-infectados ou não por S. venezuelensis (SV) e/ou Mycobacterium bovis-BCG (MB), em dois pontos das duas infecções, denominados como ponto 1 (4° e 7° dia pós-imunização [dpi]) e ponto 2 (7° e 10° dpi) por MB e SV, respectivamente. Os animais foram infectados com 700 larvas de SV pela via subcutânea e, após 3 dias, com 1x106 UFC de MB cepa selvagem pela via intravenosa. Realizou-se a quantificação do número de ovos e vermes, a dosagem de citocinas (IFN-γ, IL-4 e IL-10) e quimiocinas (CCL2 e CCL5), o envolvimento de MPO e EPO, a detecção da infecção pelo MB por PCR, a avaliação histopatológica e a expressão de moléculas coestimulat órias/imunomodulatórias (CD80, CD86, CD28, CTLA-4 e CD25) em células ou tecidos do pulmão dos animais infectados e/ou co-infectados. Os resultados mostraram que a presença do MB favoreceu para o aumento do número de ovos e vermes do SV observados nos animais nos dias 4° e 7° (ponto 1) e 7° e 10° (ponto 2) após a infecção por MB e SV, respectivamente, nos animais co-infectados (COIN). A reação de PCR foi efetiva em detectar a presença do MB no pulmão dos animais. Foi observado um aumento de IFN-γ e uma diminuição de IL-4 e EPO no pulmão dos animais do grupo COIN, além de aumento na expressão da molécula co-estimulatória CD80 no ponto 1 e uma diminuição no ponto 2. Houve uma alta produção de IL-10 no pulmão dos animais dos grupos MB e COIN, sendo que a histopatologia neste sítio mostrou formação de granulomas com grande influxo de neutrófilos, macrófagos e células epitelóides na periferia nos pulmões dos animais do grupo MB e um granuloma bem mais avançado, com centro necrótico nos animais do grupo COIN. Baseado nesses resultados, conclui-se que o MB modula a infecção pelo SV, fazendo com que os animais fiquem mais suscetíveis à infecção helmíntica. Por outro lado, o SV modula a infecção pelo MB, fazendo com haja uma modificação na formação de granuloma no pulmão dos animais do grupo COIN no ponto 1 da infecção pelo MB, que poderia ser justificada pela diminuição de IL-4 nos animais do grupo COIN.
A rising number of people have been contracting tuberculosis around the world even though a multitude of reports involving a modulation of the immune response to Mycobacterium have been published. The response to Mycobacterium is mainly mediated by Th1 lymphocytes through IFN-gamma production. Parasitic diseases account for a large proportion of human morbidity and mortality, considering the number of people affected by them and several pathologies associated to parasitic infection. Helminthic infections drive towards Th2 response which leads to IL-4, IL5 and IL-13 production. The present study evaluated the immune response of coinfected animals or not with Strongyloides venezuelensis (SV) and Mycobacterium bovis-BCG (MB) on pulmonary cells collected from BALB/c mice at time points 1 (4th and 7th days post-immunization [dpi] by MB and SV, respectively) and 2 (7th and 10th dpi by MB and SV, respectively). Animals were infected with 700 SV larvae subcutaneously, and 3 days after, 1x106 CFU of wild MB strain intravenously. The number of worms and eggs was counted as well as cytokine (IFN-gamma, IL-4 and IL-10) and chemokine (CCL2 and CCL5) assessments, and the MPO and EPO levels determination on pulmonary tissue from infected and/or coinfected animals. In addition, PCR for MB detection, the histopathology and the expression of costimulatory molecules such as CD80, CD86, CD28, CTLA-4 and CD25 on pulmonary tissue were also assessed. The results pointed that MB led to increase SV parasite burden in coinfected mice (COIN) at both time points analyzed. The PCR technique detected effectively MB. Moreover, elevated IFN-gamma and reduced IL-4 and EPO levels were detected on pulmonary tissue in the COIN group. In regard to CD80 molecule, there was an increased expression at time point 1 and diminished expression at time point 2. Also, higher amounts of IL-10 were found on pulmonary tissue in MB and COIN groups. The histopathological analysis revealed pulmonary granulomas with a number of neutrophils, macrophages and epithelial cells-like in the MB group as well as granulomas in an advanced stage with caseous necrosis in the COIN group. Based on these findings, it may be concluded that MB modulated the immune response to SV, leading coinfected animals to be more susceptible to helminthic infection. On the other hand, SV modulated the MB infection by modifying the characteristics of the pulmonary granulomas in the COIN group at time point 1 probably due the reduced IL-4 production in this group.
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Lopes, Fernando Henrique Azevedo. "NÃveis sÃricos de interleucina-6 e polimorfismo - 174G>C em infecÃÃo latente pelo Mycobacterium tuberculosis". Universidade Federal do CearÃ, 2012. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=7533.
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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel SuperiorA interleucina-6 (IL-6) à uma importante citocina que exerce papel fundamental na imunopatogÃnese de diversas doenÃas infecciosas. O objetivo deste estudo foi investigar o nÃvel de produÃÃo sistÃmica de IL-6 e aferir o papel funcional do polimorfismo -174 G>C do gene dessa citocina em indivÃduos diagnosticados como portadores de infecÃÃo latente pelo Mycobacterium tuberculosis (ILTB). Para controle, foram utilizados dois grupos de comparaÃÃo: um deles composto por portadores de tuberculose pulmonar ativa (TB) e o outro formado por indivÃduos saudÃveis, doadores de sangue. O grupo ILTB foi composto por 15 indivÃduos, selecionados dentre os contactantes de portadores de TB pulmonar ativa, atendidos no Hospital SÃo Josà de DoenÃas Infecciosas e no Centro de SaÃde da FamÃlia AnastÃcio MagalhÃes. O grupo TB foi formado por 38 pacientes com TB pulmonar ativa, procedentes do Hospital de Messejana, Hospital de Maracanaà e Hospital Geral Dr. CÃsar Cals. O grupo de indivÃduos saudÃveis contava com 63 doadores voluntÃrios de sangue do Centro de Hematologia e Hemoterapia do CearÃ. A dosagem sÃrica de IL-6 foi realizada por meio de um ensaio imunoenzimÃtico (ELISA), com kit especÃfico fornecido pela Invitrogen Corporation. Para purificaÃÃo do DNA, foi utilizado o kit GFX Genomic Blood DNA Purification, da GE Healthcare. O polimorfismo -174GC do gene da IL â 6 foi tipificado pela tÃcnica de reaÃÃo em cadeia da polimerase (PCR), utilizando-se iniciadores de sequÃncia especÃfica (PCR-SSP) (One-Lambda). As medianas de concentraÃÃes sÃricas de IL-6 para os grupos ILTB, TB e saudÃveis foram de, respectivamente, 1,7 pg/mL, 4,3 pg/mL e 0,5 pg/mL (p < 0,0001). Nos trÃs grupos estudados, o genÃtipo encontrado com maior frequÃncia foi o G/G [ILTB = (80%); TB = (58,9%); saudÃveis = (62,8%)]. Em conclusÃo, podemos inferir que a IL-6 deve desempenhar um papel importante na manutenÃÃo do estado de latÃncia, haja vista que sua concentraÃÃo, nos indivÃduos com ILTB, foi 3,4 vezes maior que no grupo saudÃvel. Ademais, constatamos que, na populaÃÃo estudada, o polimorfismo -174GC nÃo se mostrou funcional no Ãmbito da infecÃÃo latente pelo Mycobacterium tuberculosis.
Interleukin-6 (IL-6) is an important cytokine involved in the pathogenesis of multiple infectious diseases. The aim of this study was to investigate the levels of IL-6 production and to correlate to the -174G>C polymorphism at the IL-6 gene in latent infection with M. tuberculosis (ILTB). As controls, two groups were used. One of them with active pulmonary tuberculosis (TB) patients and the other with healthy blood donors. ILTB group was composed by 15 individuals, selected among active pulmonary TB contacts seen at the Hospital SÃo Josà de DoenÃas Infecciosas and the Centro de SaÃde da FamÃlia AnastÃcio MagalhÃes. TB group had 38 patients with active pulmonary disease seen at the Hospital de Messejana, Hospital de Maracanaà and the Hospital Geral Dr. CÃsar Cals. The third group was composed by 63 healthy blood donors from the Centro de Hematologia e Hemoterapia do CearÃ. Serum levels of IL-6 were measured by an ELISA using specific kits from Invitrogen Corporation. For DNA purification a GFX Genomic Blood DNA Purification kit (GE Healthcare) was used. The -174GC polymorphism was analyzed by a SSP-PCR method using One-Lambda kits. Median values of serum levels of IL-6 from ILTB, TB and healthy groups were, respectively, 1.7 pg/mL, 4.3 pg/mL and 0.5 pg/mL (p < 0.0001). For the three studied group, the most frequent genotype found was the G/G (ILTB = 80%; TB = 58.9%; saudÃveis = 62.8%). In conclusion, it is possible to consider that IL-6 should play an important role in the maintenance of latent infection state as its concentrations were 3.4 fold higher in ILTB group than that of healthy controls. Moreover, the -174GC polymorpism was not functional in the ILTB group.
Książki na temat "M. tuberculosis Infection"
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Borodulina, Elena, Elena Yakovleva, Boris Borodulin, Vladimir Mishin i Anna Mordyk. Iron metabolism in HIV-associated lung diseases - disseminated tuberculosis and pneumocystis pneumonia. ru: INFRA-M Academic Publishing LLC., 2023. http://dx.doi.org/10.12737/1932263.
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The monograph presents a comparative study of the clinical features and the main indicators of iron metabolism in lung diseases, which are AIDS-indicator diseases. The leading secondary diseases in HIV, which are often the first manifestations of HIV infection, are pneumonia caused by an opportunistic fungal infection P. jirovecii (pneumocystis pneumonia) and a specific pathogen M. tuberculosis (tuberculosis), and in both diseases it is possible to develop a dissemination syndrome. The use of iron metabolism indicators as parameters of the comparative analysis of these diseases is presented for the first time. Studies of patients with pulmonary tuberculosis and pneumocystis pneumonia in combination with HIV infection are presented.
It is intended for pulmonologists, infectious diseases specialists, phthisiologists, general practitioners.
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Eastwood, John, Cathy Corbishley i John Grange. Mycobacterial infections. Redaktor Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0196.
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The genus Mycobacterium contains over a hundred species including the M. tuberculosis complex and M. leprae, the causative agents of, respectively, tuberculosis and leprosy. The many other species are environmental saprophytes, present particularly in free and piped water sources, and some species are causes of opportunist disease in humans, especially in those who are immune compromised.The genitourinary tract is a common site of both primary and post-primary tuberculosis. In most cases of renal tuberculosis there are gross lesions consisting of caseating granulomas from which tubercle bacilli enter the urinary tract, often with the development of secondary lesions in the ureters, bladder, epididymis, and testis. Tuberculous interstitial nephritis is a less common condition with an insidious course and may result in renal failure. The urine is often negative for tubercle bacilli, emphasizing the need for biopsy in those with renal insufficiency.The risk of developing pulmonary or disseminated tuberculosis after infection is greatly enhanced by any form of immune compromise including renal failure and post-renal transplant immunosuppression.
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Hansoti, Bhakti. Pulmonary Tuberculosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0028.
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Mycobacterium tuberculosis (TB) is most commonly known for its manifestations in the lungs; symptoms include fever and chest pain (retrosternal pain and/or dull intracapsular pain). In the reactivation stage of TB, typical symptoms may include cough, weight loss, fatigue, fever, night sweats, chest pain, dyspnea, and/or hemoptysis. Symptoms may remain undiagnosed for several years. Poverty, HIV, and drug resistance are major contributors to the resurging global TB epidemic. Two kinds of tests are used to detect TB: the tuberculin skin test or a TB blood test. These tests only tell you if a person has been infected with the bacteria. The do not differentiate between latent TB infection and active TB. This distinction clinically suspected when the clinical picture of active TB matches with initial investigations (such as acid-fast bacilli stains, chest x-ray, or CT) and is definitively confirmed by the growth of M. tuberculosis in a clinical specimen.
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Abdulkader, Rita, i Richard A. Watts. Mycobacterial diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0103.
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The main diseases caused by mycobacterial infection are tuberculosis (TB) and leprosy. Despite a fall in the prevalence of these diseases over the last decade, they are still significant causes of morbidity and mortality worldwide. Atypical mycobacterial infections are encountered less frequently. Immigration patterns, the frequency of human immunodeficiency infection, and the increased numbers of patients on immunosuppressive treatments render mycobacterial infections relevant not only to physicians in the developing world where they traditionally occurred but also in the developed world. Skeletal TB occurs in 1–3% of cases of TB infection, and is more frequently encountered in the immunocompromised. A high index of suspicion is required, diagnosis relies on a combination of clinical features and radiological, histological, and microbiological tests. Multidrug regimens are required for treatment with surgery in selected cases. Leprosy is caused by M. leprae infection. The disease is still a leading cause of disability worldwide. Diagnosis is usually clinical. The course of the disease is indolent but may be interrupted by acute inflammatory reactions, which contribute to nerve damage and disability. Treatment aims at eliminating the mycobacteria using multidrug regimens, and management of complications including leprosy reactions and long-term nerve damage. Atypical mycobacterial infections affecting bone and joints are uncommon; they usually follow direct inoculation of the pathogen. Haematogenous dissemination is encountered in immunocompromised patients. These microorganisms are not usually susceptible to the same drug regimens used in the treatment of tuberculosis.
Części książek na temat "M. tuberculosis Infection"
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Kusner, David. "Analysis of Macrophage Signaling Following M. tuberculosis Infection". W Tuberculosis, 77–101. London: Taylor & Francis, 2022. http://dx.doi.org/10.1201/9780429091063-3.
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Boakye-Appiah, Justice, Belinda Hall, Rajko Reljic i Rachel E. Simmonds. "Current Progress and Prospects for a Buruli Ulcer Vaccine". W Vaccines for Neglected Pathogens: Strategies, Achievements and Challenges, 71–95. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-24355-4_5.
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AbstractBuruli ulcer (BU), one of the skin-related neglected tropical diseases (skin NTDs), is a necrotizing and disabling cutaneous disease caused by subcutaneous infection with Mycobacterium ulcerans. Leading on from the World Health Organization’s (WHO) establishment of a global BU initiative in 1998, >67,000 cases of BU have been reported from over 32 countries, mostly from West Africa and Australia. While treatment is currently in the transition period from rifampicin plus streptomycin (injection) to an all-oral regimen, it cannot hope to eradicate this opportunistic environmental pathogen. M. ulcerans is genetically very similar to related pathogenic organisms M. marinum, M. leprae and M. tuberculosis. However, M. ulcerans carries a unique megaplasmid, pMUM001, encoding the biosynthetic machinery responsible for production of a lipid-like exotoxin virulence factor, mycolactone. This diffusible compound causes the substantial divergence in BU’s pathogenic aetiology from other mycobacterial infections. Hence, mycolactone is cytotoxic and immunosuppressive and causes vascular dysfunction in infected skin. A major recent advance in our understanding of BU pathogenesis has been agreement on the mycolactone’s mechanism of action in host cells, targeting the Sec61 translocon during a major step in secretory and membrane protein biogenesis. While vaccine development for all mycobacteria has been challenging, mycolactone production likely presents a particular challenge in the development of a BU vaccine. The live-attenuated vaccine BCG is known to provide only partial and transient protection in humans but provides a convenient baseline in mouse preclinical studies where it can delay, but not prevent, disease progression. No experimental vaccine strategy has yet conferred greater protection than BCG. However, there is now the prospect of developing a vaccine against mycolactone itself, which may provide hope for the future.
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Kaufmann, Stefan H. E., i Gennaro De Libero. "Cytolytic Cells in M. tuberculosis Infections". W Infectious Agents and Pathogenesis, 151–70. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5418-5_7.
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Wallis, Robert S., i Jerrold J. Ellner. "Immunology of M. tuberculosis and Other Mycobacteria". W Pulmonary Infections and Immunity, 129–48. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-1063-9_8.
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Sultzer, Barnet M. "Polyclonal Lymphocyte Activation by M. tuberculosis and Its Products". W Infectious Agents and Pathogenesis, 277–304. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5418-5_13.
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Kato, Kazuyuki, i Ken-Ichi Yamamoto. "Role of Adjuvant and Immunogenic Moieties of M. tuberculosis in Pathogenicity". W Infectious Agents and Pathogenesis, 39–58. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5418-5_2.
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Agrawal, Ruchi, Vignesh H. Narayan i Deepak Kumar Saini. "Two-Component Signalling Systems of M. tuberculosis: Regulators of Pathogenicity and More". W Dynamic Models of Infectious Diseases, 79–109. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9224-5_4.
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Buschman, Ellen, i Emil Skamene. "Genetic Background of the Host and Expression of Natural Resistance and Acquired Immunity to M. tuberculosis". W Infectious Agents and Pathogenesis, 59–79. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5418-5_3.
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Chaisson, Richard E., i Jean B. Nachega. "Tuberculosis". W Oxford Textbook of Medicine, redaktor Christopher P. Conlon, 1126–49. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0130.
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Tuberculosis is caused by organisms of the Mycobacterium tuberculosis complex, including M. tuberculosis (the most important), M. bovis, and M. africanum. It has been present since antiquity and is the leading infectious cause of death ahead of HIV infection. An estimated 2 billion people worldwide carry latent infection, when M. tuberculosis persists within cells and granulomas, with the potential to reactivate to cause disease decades later. Tubercle bacilli are transmitted between people by aerosols generated when an infectious person coughs. Proximity to an infectious person determines the risk of infection. Host immunity and factors affecting it—most importantly HIV infection but also diabetes, cigarette smoking, and alcohol and drug abuse—determine the risk of active disease following infection.
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Chaisson, Richard E., i Jean B. Nachega. "Tuberculosis". W Oxford Textbook of Medicine, 810–31. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.070625_update_001.
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Tuberculosis is caused by organisms of the Mycobacterium tuberculosis complex, including M. tuberculosis (the most important), M. bovis, and M. africanum. It has been present since antiquity and is the second leading infectious cause of death after HIV infection. An estimated 2 billion people worldwide carry latent infection, when ...
Streszczenia konferencji na temat "M. tuberculosis Infection"
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Andrews, Jason R., Farzad Noubary, Rochelle P. Walensky, Elena Losina i C. Robert Horsburgh. "Decreased Progression To Active Tuberculosis Following Re-Infection With M. Tuberculosis". W 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.a1840.
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PAVAN, THAIS ROHDE, MURIEL MANICA, MONICA MANICA, SABRINA NALIN i GUILHERME TONET. "PERITONEAL TUBERCULOSIS IN INFLIXIMAB USER AFTER NEGATIVE SCREENING FOR LATENT INFECTION BY M. TUBERCULOSIS". W 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-202.
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May, Elebeoba, Andrei Leitao, Jean-Loup Faulon, Jaewook Joo, Milind Misra i Tudor I. Oprea. "Understanding virulence mechanisms in M. tuberculosis infection via A circuit-based simulation framework". W 2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2008. http://dx.doi.org/10.1109/iembs.2008.4650325.
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Karpina, Natalya, Artem Dudchenko, Elena Larionova i Atadzhan Ergeshov. "The peculiarities of drug susceptibility of M. tuberculosis isolated from patients with late-stage HIV infection". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2993.
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Fiske, Christina, Alexandre S. de Almeida, Spyros A. Kalams i Timothy R. Sterling. "Abnormal Immune Responses In Persons With Previous Extrapulmonary Tuberculosis In An In Vitro Macrophage Model That Simulates In Vivo Infection With M. Tuberculosis". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3218.
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Smith, Rachel M., Adithya Cattamanchi, John Metcalfe, Karen Steingart, Philip C. Hopewell i Madhukar Pai. "Systematic Review Of Sensitivity Of Interferon-gamma Release Assays For Detection Of M. Tuberculosis Infection In HIV-infected Patients". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2264.
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de Almeida, Alexandre S., Christina Fiske, Timothy R. Sterling i Spyros A. Kalams. "Previously Treated TB Patients Have A Higher Percentage Of Circulating Treg CD4+CD25highFoxP3 CD127- Cells Than Persons With Latent M. Tuberculosis Infection". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3217.
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Pompermaier, Carolina, Mateus Xavier Schenato, Tales Antunes Franzini, Fábio Biguelini Duarte i Guilherme Roloff Cardoso. "TUBERCULOUS LYMPHADENITIS: A LITERATURE REVIEW". W XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1080.
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Introduction: Lymphadenitis, also previously called “scrofula,” is the most common cause of manifestation of extrapulmonary tuberculosis (TB), an extremely prevalent disease in underdeveloped regions, causing millions of deaths around the world. This is why it must be recognized and treated as early as possible. Objective: This review aims to summarize the main topics of tuberculous lymphadenitis (TL), covering epidemiology, clinical, and recent treatments. Methods: This article consists of a review of publications on the subject. The research was carried out through SciELO, PubMed, and LILACS databases, as well as virtual scientific libraries such as DynaMed and UpToDate. Results: TL is the infection of lymph nodes caused by Mycobacterium tuberculosis, and it is the most common type of extrapulmonary TB, mainly in endemic areas. Worldwide, there is an increase in the incidence of TB in developed and underdeveloped countries, resulting in millions of deaths per year. Its relationship with HIV and the consequent development of extrapulmonary forms has been increasingly common, representing about 21% of TB cases in the United States. The main extrapulmonary TB sites are as follows: lymph nodes, pleura, meninges, bones, miliary, and disseminated. In HIV patients, atypical presentations are not uncommon. The clinical picture consists of slow lymph node growth, generally affecting the cervical region and may affect other sites; signs and symptoms of the primary TB may also be present. The diagnosis of TL is made by culture or molecular identification of M. tuberculosis in the tissue of the affected lymph node, which can be approached by excision or by fine-needle biopsy. The anatomopathological findings are giant epithelioid cells, granulomas, and caseous necrosis. Treatment should be started empirically according to the clinic, awaiting laboratory confirmation, and its first line consists of the first 2 months with RHZE (Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol), followed by 4 months of Isoniazid and Rifampicin. Paradoxical worsening after starting the therapy is one of the complications, usually occurring 8 weeks after starting the treatment. Management should be monitored on an outpatient basis, with cure occurring in up to 94% of the cases. Conclusion: TL is one of the main manifestations of extrapulmonary TB, closely related to coinfection with HIV. It should be promptly investigated in patients with a compatible clinical presentation and present in endemic areas. Its treatment, despite long duration, cures the vast majority of cases and reduces the overall morbidity and mortality of properly treated patients.
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Silva, Matheus Alves da, Eduardo Mesquita de Souza, Rafael Bragança Rodrigues Matias, Ana Luisa Vieira de Faria, Amanda Miranda de Mendonça, André Luiz Guimarães de Queiroz, Victor Hugo Rocha Marussi i Alex Machado Baeta. "Subacute fever and torpor in a hematological patient revealing atypical CLIPPERS with supratentorial involvement: a case report". W XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.403.
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Case report: A 62-year-old patient was transferred from another hospital with complaints of subacute torpor and fever two months after an allogeneic bone marrow transplant. He had the diagnosis of chronic myelomonocytic leukemia type 2 four years before the beginning of the neurological symptoms. The disease remained stable for two years after the diagnosis, but progressed and he was submitted to a bone marrow transplant. The complications during the procedure were a febrile neutropenia, that resolved with a cycle of antibiotics, and a reactivation of cytomegalovirus (CMV) infection (he had a high risk to reactivation due to the status of antibodies of the donator, that was negative, and he had positive antibodies). He remained stable and was discharged from the hospital 30 days after the transplant. Two months after the transplant, the fever and torpor began, and he went to the emergency department in his hometown. There, he was diagnosed with a positive coronavirus disease 2019 (COVID-19) infection and reactivation of cytomegalovirus, with prescription of endovenous ganciclovir, without clinical improvement. His clinical symptoms evolved to loss of balance and progressive torpor, and was transferred to our hospital for clinical evaluation. In the initial examination, he was febrile, torporous, he was not collaborative to the neurological examination due to the level of consciousness. He was hypotonic and had withdrawal from a painful stimulus on four limbs. His tendinous reflexes were hyperactive and symmetrical. Due to his level of consciousness, the cerebellar maneuvers were not testable. He was then submitted to orotracheal intubation due to neurological deterioration. In his complementary investigation, the serum polymerase chain reaction (PCR) for CMV was already negative and his PCR for COVID-19 was also negative. The electroencephalogram showed slow generalized periodic discharges. His computerized tomography showed no abnormalities, so he was submitted to a lumbar puncture that showed 8 cells, with 97% lymphocytes, 74 mg/dL of protein, 26 mg/dL of glucose with no neoplasic cells and a positive PCR for Toxoplasma gondii. The PCR for mycobacterium tuberculosis, cryptococcosis, and viruses were negative. After the results, we started sulfadiazine and pyrimethamine and he was submitted to a magnetic resonance imaging that showed multiple nodular foci of hypersignal in T2/FLAIR (T2-weighted-Fluid-Attenuated Inversion Recovery) and diffusion abnormalities on the cortical surface of the cerebellar hemispheres, thalamus, basal ganglia and subcortical white matter of the cerebral hemispheres, being more evident in the cerebellum and basal ganglia. Besides the atypical radiological findings for neurotoxoplasmosis, his serologic testing on the serum showed an positive immunoglobulin M and immunoglobulin G for Toxoplasma gondii. He had no clinical improvement with the antibiotics, and so, ten days after he was submitted to a new magnetic resonance imaging showing increase in the size and number of multiple small focal lesions with hypersignal on T2/FLAIR in the brain parenchyma, highlighting confluent lesions in the basal ganglia and focal lesions in the cerebellar hemispheres, which show contrast uptake, as well as in the thalamus and midbrain. His neurological symptoms evolved and he showed a minimally conscious state, with spasticity in the four limbs. He was submitted to a new lumbar puncture that showed 1 cell, 78 mg/dL of protein and 50 mg/dl of glucose, an improvement, despite clinical and radiological worsening. Because of the clinical worsening, he was submitted to a brain biopsy. His cerebral biopsy was negative for neoplasic infiltration of the cerebral nervous system, viral infections, cryptococcus and toxoplasmosis. It showed an interstitial CD3 lymphocytic inflammation with vasculitis and frequent macrophages, very rare CD20 lymphocytes and p24 and SV-40 negative. His neuropathological criteria were compatible with CLIPPERS (chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids). The patient was submitted to five days of metilprednisolone and with oral prednisone after, with slow clinical improvement, but probably due to the lack of systemic clinical status of the patient and delayed diagnosis because of the atypical presentation, the patient died of pneumonia.