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1
A, Abdelmoktader. "Mycobacterial Tuberculosis Epidemiology and Pathogenesis." Virology & Immunology Journal 4, no. 4 (2020): 1–7. http://dx.doi.org/10.23880/vij-16000259.
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Mycobacterium tuberculosis (MTB) is an acid fast bacterium (AFB); it has tough cell wall and circular chromosome. It is transmitted through the airborne route and cause tuberculosis (TB). The distribution of tuberculosis is not uniform across the globe; about 80% of the population in many Asian and African countries and it is the second most common cause of death from infectious disease after HIV. Organisms deposited mainly in the upper lung zones, kidneys and bones. In persons with intact cell-mediated immunity (CMI), collections of activated T cells and macrophages form granulomas that limit multiplication and spread of the organism. The Status of CMI will determine if the patient will get active or latent TB infection.
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Martinez-Garcia, M. A., W.-J. Guan, D. de-la-Rosa, et al. "Post-TB bronchiectasis: from pathogenesis to rehabilitation." International Journal of Tuberculosis and Lung Disease 27, no. 3 (2023): 175–81. http://dx.doi.org/10.5588/ijtld.22.0566.
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The destruction of lung parenchyma caused by TB can result in pulmonary sequelae that are classified as bronchiectasis due to traction (radiological sequelae), and bronchiectasis persisting with an inflammatory bronchial component and opportunistic bronchial infection. There is a lack of studies that comprehensively analyse whether post-TB bronchiectasis differs in clinical, prognostic or therapeutic aspects from bronchiectasis arising from other aetiologies. However, it has been noted that post-TB bronchiectasis tends to appear more frequently in the upper lung lobes. In many countries, TB is the most frequent known cause of bronchiectasis, but there is currently no targeted management of bronchiectasis due to TB as opposed to other aetiologies. It is imperative to first prevent TB, and when that fails to provide early diagnosis and adequate treatment for TB disease. In addition, efforts should be made to limit additional lung insults such as tobacco use and provide management of post TB bronchiectasis to minimise further pulmonary sequelae. The objective of this minireview was to provide an update on post-TB bronchiectasis, its definition, epidemiological data, pathophysiology, and clinical, diagnosis and therapeutic aspects.
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Gergert, V. Ja, M. M. Averbakh, and A. E. Ergeshov. "Immunological aspects of tuberculosis pathogenesis." Terapevticheskii arkhiv 91, no. 11 (2019): 90–97. http://dx.doi.org/10.26442/00403660.2019.11.000262.
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The morphological aspects of TB pathogenesis are well described in the publications. Much is also known about the main stages of development and formation of specific adaptive immunity. However, from our point of view, not enough attention is being paid to the involvement of the immune system in the pathogenesis of clinically relevant TB abnormalities, as well as various forms of the disease. Nevertheless, there is no doubt that the variety of clinical manifestations of any disease associated with the penetration of a foreign agent into the body, and Mycobacterium tuberculosis (MTB) in particular, is due to the collective interaction of the infectious agent and the individual response of the macroorganism to this infectious agent. The mosaic of such interactions usually imposes its own adjustments on the development of different forms of the process, its speed and direction, as well as the outcomes. Certainly, the response of a macroorganism to MTB is an integral part of pathogenesis and consists of many general components including the responses associated with the mechanisms of natural and acquired immunity. Intensity of these reactions depends on the characteristics of an agent (MTB) and a macroorganism. For the development of TB disease, massiveness of TB infection, dose and duration of MTB exposure to the human body, as well as virulence of MTB and the level of body's protection during the exposure play a very important role. TB pathogenesis is somewhat different in primary MTB infection and re - infection. With primary infection, 88-90% of individuals do not have clinical manifestations, and only the tuberculin skin test conversion signals the onset of infection. In some cases, without any use of anti-TB drugs limited abnormalities may result in spontaneous cure with the minimal residual changes in the lungs, intrathoracic lymph nodes and tissues of other organs, often in the form of calcifications and limited areas of fibrosis in more advanced cases. Only 10-12% of newly infected individuals develop TB with severe clinical manifestations requiring TB therapy. The absence of clinical manifestations of primary TB infection can be explained by a high level of natural resistance of the human body to tuberculosis, and sometimes can be an effect of acquired protection due to BCG vaccination. This review attempts to discuss the role of immune mechanisms in the pathogenesis both at the beginning of disease development, and in the process of its various manifestations. Issues of genetically determined resistance or susceptibility to TB are not being covered in detail in this manuscript.
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Malikova, O. G., O. G. Komissarova, N. V. Chumovatov, and A. E. Ergeshov. "PULMONARY TB COMPLICATED BY TRACHEOBRONCHIAL TB." Вестник ЦНИИТ 7, no. 4 (2023): 12–22. http://dx.doi.org/10.57014/2587-6678-2023-7-4-12-22.
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In the recent years we have observed a positive tendency towards better epidemiological rates of TB in the Russian Federation. Incidence and mortality rates fell to a record low. However, a share of patients with advanced or complicated pulmonary TB increased. Our review highlights epidemiological data, pathogenesis, clinical manifestations, diagnostics, and management of pulmonary TB complicated by tracheobronchial TB nowadays.
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Jones, Christine, Elizabeth Whittaker, Alasdair Bamford, and Beate Kampmann. "Immunology and pathogenesis of childhood TB." Paediatric Respiratory Reviews 12, no. 1 (2011): 3–8. http://dx.doi.org/10.1016/j.prrv.2010.09.006.
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Sinigaglia, Alessandro, Elektra Peta, Silvia Riccetti, Seshasailam Venkateswaran, Riccardo Manganelli, and Luisa Barzon. "Tuberculosis-Associated MicroRNAs: From Pathogenesis to Disease Biomarkers." Cells 9, no. 10 (2020): 2160. http://dx.doi.org/10.3390/cells9102160.
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Tuberculosis (TB) caused by Mycobacterium tuberculosis is one of the most lethal infectious diseases with estimates of approximately 1.4 million human deaths in 2018. M. tuberculosis has a well-established ability to circumvent the host immune system to ensure its intracellular survival and persistence in the host. Mechanisms include subversion of expression of key microRNAs (miRNAs) involved in the regulation of host innate and adaptive immune response against M. tuberculosis. Several studies have reported differential expression of miRNAs during active TB and latent tuberculosis infection (LTBI), suggesting their potential use as biomarkers of disease progression and response to anti-TB therapy. This review focused on the miRNAs involved in TB pathogenesis and on the mechanism through which miRNAs induced during TB modulate cell antimicrobial responses. An attentive study of the recent literature identifies a group of miRNAs, which are differentially expressed in active TB vs. LTBI or vs. treated TB and can be proposed as candidate biomarkers.
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Alsayed, Shahinda S. R., and Hendra Gunosewoyo. "Tuberculosis: Pathogenesis, Current Treatment Regimens and New Drug Targets." International Journal of Molecular Sciences 24, no. 6 (2023): 5202. http://dx.doi.org/10.3390/ijms24065202.
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Mycobacterium tuberculosis (M. tb), the causative agent of TB, is a recalcitrant pathogen that is rife around the world, latently infecting approximately a quarter of the worldwide population. The asymptomatic status of the dormant bacteria escalates to the transmissible, active form when the host’s immune system becomes debilitated. The current front-line treatment regimen for drug-sensitive (DS) M. tb strains is a 6-month protocol involving four different drugs that requires stringent adherence to avoid relapse and resistance. Poverty, difficulty to access proper treatment, and lack of patient compliance contributed to the emergence of more sinister drug-resistant (DR) strains, which demand a longer duration of treatment with more toxic and more expensive drugs compared to the first-line regimen. Only three new drugs, bedaquiline (BDQ) and the two nitroimidazole derivatives delamanid (DLM) and pretomanid (PMD) were approved in the last decade for treatment of TB—the first anti-TB drugs with novel mode of actions to be introduced to the market in more than 50 years—reflecting the attrition rates in the development and approval of new anti-TB drugs. Herein, we will discuss the M. tb pathogenesis, current treatment protocols and challenges to the TB control efforts. This review also aims to highlight several small molecules that have recently been identified as promising preclinical and clinical anti-TB drug candidates that inhibit new protein targets in M. tb.
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Quinn, Carson M., Victoria Poplin, John Kasibante, et al. "Tuberculosis IRIS: Pathogenesis, Presentation, and Management across the Spectrum of Disease." Life 10, no. 11 (2020): 262. http://dx.doi.org/10.3390/life10110262.
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Antiretroviral therapy (ART), while essential in combatting tuberculosis (TB) and HIV coinfection, is often complicated by the TB-associated immune reconstitution inflammatory syndrome (TB-IRIS). Depending on the TB disease site and treatment status at ART initiation, this immune-mediated worsening of TB pathology can take the form of paradoxical TB-IRIS, unmasking TB-IRIS, or CNS TB-IRIS. Each form of TB-IRIS has unique implications for diagnosis and treatment. Recently published studies have emphasized the importance of neutrophils and T cell subtypes in TB-IRIS pathogenesis, alongside the recognized role of CD4 T cells and macrophages. Research has also refined our prognostic understanding, revealing how the disease can impact lung function. While corticosteroids remain the only trial-supported therapy for prevention and management of TB-IRIS, increasing interest has been given to biologic therapies directly targeting the immune pathology. TB-IRIS, especially its unmasking form, remains incompletely described and more data is needed to validate biomarkers for diagnosis. Management strategies remain suboptimal, especially in the highly morbid central nervous system (CNS) form of the disease, and further trials are necessary to refine treatment. In this review we will summarize the current understanding of the immunopathogenesis, the presentation of TB-IRIS and the evidence for management recommendations.
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Arshad, Aysha, Sujay Dayal, Raj Gadhe, et al. "Analysis of Tuberculosis Meningitis Pathogenesis, Diagnosis, and Treatment." Journal of Clinical Medicine 9, no. 9 (2020): 2962. http://dx.doi.org/10.3390/jcm9092962.
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Tuberculosis (TB) is the most prevalent infectious disease in the world. In recent years there has been a significant increase in the incidence of TB due to the emergence of multidrug resistant strains of Mycobacterium tuberculosis (M. tuberculosis) and the increased numbers of highly susceptible immuno-compromised individuals. Central nervous system TB, includes TB meningitis (TBM-the most common presentation), intracranial tuberculomas, and spinal tuberculous arachnoiditis. Individuals with TBM have an initial phase of malaise, headache, fever, or personality change, followed by protracted headache, stroke, meningismus, vomiting, confusion, and focal neurologic findings in two to three weeks. If untreated, mental status deteriorates into stupor or coma. Delay in the treatment of TBM results in, either death or substantial neurological morbidity. This review provides latest developments in the biomedical research on TB meningitis mainly in the areas of host immune responses, pathogenesis, diagnosis, and treatment of this disease.
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DRUSZCZYŃSKA, MAGDALENA, MAGDALENA KOWALEWICZ-KULBAT, MAREK FOL, MARCIN WŁODARCZYK, and WIESŁAWA RUDNICKA. "Latent Mycobacterium tuberculosis Infection – Pathogenesis, Diagnosis, Treatment and Prevention Strategies." Polish Journal of Microbiology 61, no. 1 (2012): 3–10. http://dx.doi.org/10.33073/pjm-2012-001.
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One third of the earths population is infected with Mycobacterium tuberculosis (Mtb), but only 5-10% of the infected individuals develop active tuberculosis (TB) over their lifetime. The remaining 90-95% stay healthy and are called latently infected individuals. They are the biggest reservoir of the tubercle bacilli and identifying the cases of latent TB is a part of the global plan of TB control. From the clinical point of view detection of latent TB infections (LTBI) in individuals with the highest active TB risk including cases of HIV infection, autoimmune inflammatory diseases or cancer, is a priority. This review summarizes the recent findings in the pathogenesis of latent TB, its diagnosis, treatment and prevention.
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Hunter, Robert L. "The Pathogenesis of Tuberculosis–The Koch Phenomenon Reinstated." Pathogens 9, no. 10 (2020): 813. http://dx.doi.org/10.3390/pathogens9100813.
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Research on the pathogenesis of tuberculosis (TB) has been hamstrung for half a century by the paradigm that granulomas are the hallmark of active disease. Human TB, in fact, produces two types of granulomas, neither of which is involved in the development of adult type or post-primary TB. This disease begins as the early lesion; a prolonged subclinical stockpiling of secreted mycobacterial antigens in foamy alveolar macrophages and nearby highly sensitized T cells in preparation for a massive necrotizing hypersensitivity reaction, the Koch Phenomenon, that produces caseous pneumonia that is either coughed out to form cavities or retained to become the focus of post-primary granulomas and fibrocaseous disease. Post-primary TB progresses if the antigens are continuously released and regresses when they are depleted. This revised paradigm is supported by nearly 200 years of research and suggests new approaches and animal models to investigate long standing mysteries of human TB and vaccines that inhibit the early lesion to finally end its transmission.
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Glassman, Ira, Kevin H. Nguyen, Jane Giess, Cheldon Alcantara, Michelle Booth, and Vishwanath Venketaraman. "Pathogenesis, Diagnostic Challenges, and Risk Factors of Pott’s Disease." Clinics and Practice 13, no. 1 (2023): 155–65. http://dx.doi.org/10.3390/clinpract13010014.
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Tuberculosis (TB) prevalence is increasing in developed nations and continuing to cause significant mortality in low- and middle-income countries. As a result of the uptick in cases, there also exists an increased prevalence of extrapulmonary TB. TB is caused by Mycobacterium tuberculosis (M. tb). When M. tb disseminates to the vertebral column, it is called Pott’s disease or spinal TB. The frequency, symptoms, and severity of the disease range by the location of the spine and the region of the affected vertebrae. While the current literature shows that timely diagnosis is crucial to reduce the morbidity and mortality from Pott’s disease, there is a lack of specific clinical diagnostic criteria for Pott’s disease, and the symptoms may be very non-specific. Studies have shown that novel molecular diagnostic methods are effective and timely choices. Research has implicated the risk factors for the susceptibility and severity of Pott’s disease, such as HIV and immunosuppression, poverty, and malnutrition. Based on the current literature available, our group aims to summarize the pathogenesis, clinical features, diagnostic challenges, as well as the known risk factors for Pott’s disease within this literature review.
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Fisher, Kimone L., Kerishka Rajkumar-Bhugeloo, Denelle Moodley, et al. "Investigating neutrophil cell death in TB pathogenesis." Gates Open Research 5 (April 29, 2022): 175. http://dx.doi.org/10.12688/gatesopenres.13472.2.
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Background: Neutrophils are one of the major early role players in antimycobacterial immunity. Upon infection, neutrophils can undergo NETosis, a cell death characterized by release of neutrophil extracellular traps (NETs). The role of NETosis in TB progression remains poorly characterized. We aim to characterize mechanisms underlying NETosis during TB pathogenesis by identifying genes that drive the cell death, and to determine their potential as markers of disease progression in high-risk individuals. Finally, we intend to evaluate neutrophil associated genes as targets for host directed therapy to reduce pathological damage caused by NETosis. Methods: Quantitative PCR will be used to quantify expression of specific genes identified in the blood of individuals with active lung disease (n=30), compared to those from healthy (n=30) and latently infected individuals (LTBI) (n=30). In addition, temporal events associated with NETosis will be measured using live microscopy in a neutrophil in vitro model of Mycobacterium tuberculosis (Mtb) infection. Candidate genes found to be associated with NETosis will be targeted with pharmaceutical inhibitors. Conclusion: Genes associated with neutrophil mediated cell death may serve as potential biomarkers of pathological damage and disease progression, as well as targets for host-directed therapy.
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Fisher, Kimone L., Kerishka Rajkumar-Bhugeloo, Denelle Moodley, et al. "Investigating neutrophil cell death in TB pathogenesis." Gates Open Research 5 (December 7, 2021): 175. http://dx.doi.org/10.12688/gatesopenres.13472.1.
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Background: Neutrophils are one of the major early role players in antimycobacterial immunity. Upon infection, neutrophils can undergo NETosis, a cell death characterized by release of neutrophil extracellular traps (NETs). The role of NETosis in TB progression remains poorly characterized. We aim to characterize mechanisms underlying NETosis during TB pathogenesis by identifying genes that drive the cell death, and to determine their potential as markers of disease progression in high-risk individuals. Finally, we intend to evaluate neutrophil associated genes as targets for host directed therapy to reduce pathological damage caused by NETosis. Methods: Quantitative PCR will be used to quantify expression of specific genes identified in the blood of individuals with active lung disease (n=30), compared to those from healthy (n=30) and latently infected individuals (LTBI) (n=30). In addition, temporal events associated with NETosis will be measured using live microscopy in a neutrophil in vitro model of Mycobacterium tuberculosis (Mtb) infection. Candidate genes found to be associated with NETosis will be targeted with pharmaceutical inhibitors. Conclusion: Genes associated with neutrophil mediated cell death may serve as potential biomarkers of pathological damage and disease progression, as well as targets for host-directed therapy.
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Hunter, Robert, Jefrey Actor, Shen-An Hwang, et al. "Pathogenesis and Animal Models of Post-Primary (Bronchogenic) Tuberculosis, A Review." Pathogens 7, no. 1 (2018): 19. http://dx.doi.org/10.3390/pathogens7010019.
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Primary and post-primary tuberculosis (TB) are different diseases caused by the same organism. Primary TB produces systemic immunity. Post-primary TB produces cavities to support massive proliferation of organisms for transmission of infection to new hosts from a person with sufficient immunity to prevent systemic infection. Post-primary, also known as bronchogenic, TB begins in humans as asymptomatic bronchial spread of obstructive lobular pneumonia, not as expanding granulomas. Most lesions regress spontaneously. However, some undergo caseation necrosis that is coughed out through the necrotic bronchi to form cavities. Caseous pneumonia that is not expelled through the bronchi is retained to become the focus of fibrocaseous disease. No animal reproduces this entire process. However, it appears that many mammals utilize similar mechanisms, but fail to coordinate them as do humans. Understanding this makes it possible to use human tuberculous lung sections to guide manipulation of animals to produce models of particular human lesions. For example, slowly progressive and reactivation TB in mice resemble developing human bronchogenic TB. Similarly, bronchogenic TB and cavities resembling those in humans can be induced by bronchial infection of sensitized rabbits. Granulomas in guinea pigs have characteristics of both primary and post primary TB. Mice can be induced to produce a spectrum of human like caseating granulomas. There is evidence that primates can develop bronchogenic TB. We are optimistic that such models developed by coordinated study of human and animal tissues can be used with modern technologies to finally address long-standing questions about host/parasite relationships in TB, and support development of targeted therapeutics and vaccines.
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Haiga, Yuri. "Pathogenesis of tuberculous meningitis (TBM): a mini-review." Indonesia Journal of Biomedical Science 16, no. 1 (2022): 51–54. http://dx.doi.org/10.15562/ijbs.v16i1.379.
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Background: Tuberculosis (TB) is the leading cause of death from a single infectious agent (Mycobacterium tuberculosis) and killed nearly 1.5 million people in 2018. TB mostly manifests as a pulmonary disease but can also affect other parts of the body, causing extrapulmonary TB. Approximately 5% of all cases of extrapulmonary TB are tuberculous meningitis (TBM), which is caused by the spread of M. tuberculosis to the meninges and cerebrospinal fluid (CSF). Result: TBM is the most devastating form of TB and causes high rates of morbidity and mortality, with an estimated 50% of patients dying or suffering from neurological sequelae and complications. Meningitis is categorized as a medical emergency because it can cause death due to inflammation that occurs in the brain and spinal cord. Most meningitis patients present with fever, and signs and symptoms of meningeal inflammation include headache, neck stiffness and altered mental status. Disease management has limitations due to the limited availability of available diagnostic approaches. Until now, knowledge about the pathogenesis of TBM has been limited. Conclusion: Further research is urgently needed to improve understanding of disease pathogenesis and diagnostic approaches based on biomarkers of disease. Current knowledge on the pathogenesis of TBM summarize the literature on diagnostic approaches based on biomarkers, which may be useful in the management of TBM.
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Arya, Rakesh, Hemlata Shakya, Reetika Chaurasia, Md Azizul Haque, and Jong-Joo Kim. "Exploring the Role of Extracellular Vesicles in the Pathogenesis of Tuberculosis." Genes 15, no. 4 (2024): 434. http://dx.doi.org/10.3390/genes15040434.
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Tuberculosis (TB) remains a significant global health concern, necessitating accurate diagnosis and treatment monitoring. Extracellular vesicles (EVs), including exosomes, play crucial roles in disease progression, with their associated genes serving as potential biomarkers and therapeutic targets. Leveraging publicly available RNA-Seq datasets of TB patients and healthy controls (HCs), to identify differentially expressed genes (DEGs) and their associated protein–protein interaction networks and immune cell profiles, the common EV-related DEGs were identified and validated in the GSE42830 and GSE40553 datasets. We have identified nine common EV-related DEGs (SERPINA1, TNFAIP6, MAPK14, STAT1, ITGA2B, VAMP5, CTSL, CEACAM1, and PLAUR) upregulated in TB patients. Immune cell infiltration analysis revealed significant differences between TB patients and HCs, highlighting increased proportions of various immune cells in TB patients. These DEGs are involved in crucial cellular processes and pathways related to exocytosis and immune response regulation. Notably, VAMP5 exhibited excellent diagnostic performance (AUC—0.993, sensitivity—93.8%, specificity—100%), with potential as a novel biomarker for TB. The EV-related genes can serve as novel potential biomarkers that can distinguish between TB and HCs. VAMP5, which functions in exosome biogenesis and showed significant upregulation in TB, can be targeted for therapeutic interventions and treatment outcomes.
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Miggiano, Riccardo, Menico Rizzi, and Davide M. Ferraris. "Mycobacterium tuberculosis Pathogenesis, Infection Prevention and Treatment." Pathogens 9, no. 5 (2020): 385. http://dx.doi.org/10.3390/pathogens9050385.
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Tuberculosis (TB) is an infectious disease caused by the bacterium Mycobacterium tuberculosis (MTB) and it represents a persistent public health threat for a number of complex biological and sociological reasons. According to the most recent Global Tuberculosis Report (2019) edited by the World Health Organization (WHO), TB is considered the ninth cause of death worldwide and the leading cause of mortality by a single infectious agent, with the highest rate of infections and death toll rate mostly concentrated in developing and low-income countries. We present here the editorial section to the Special Issue entitled “Mycobacterium tuberculosis Pathogenesis, Infection Prevention and Treatment” that includes 7 research articles and a review. The scientific contributions included in the Special Issue mainly focus on the characterization of MTB strains emerging in TB endemic countries as well as on multiple mechanisms adopted by the bacteria to resist and to adapt to antitubercular therapies.
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Linge, I. A., and A. S. Apt. "A controversial role of neutrophils in tuberculosis infection pathogenesis." Russian Journal of Infection and Immunity 11, no. 5 (2021): 809–19. http://dx.doi.org/10.15789/2220-7619-acr-1670.
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Tuberculosis (TB) continues to be an important and unresolved medical problem. About a quarter of mankind is infected with Mycobacterium tuberculosis, and about 5–10% of these people eventually develop TB. Macrophages and CD4+ T cells are considered the key cells providing defense against TB infection. The role of neutrophils in TB is less well defined. Neutrophils are short-lived granulocytes among first migrate into the infectious lung tissue and phagocy tose mycobacteria. On the one hand, there is evidence for protective role of neutrophils in TB released via anti-microbial peptides inhibiting mycobacterial growth, up-regulation of CD4+ T-cell activation, and dendritic cell migration in the lymph nodes. On the other hand, infection of genetically TB susceptible animals leads to an overwhelming lung neutrophil inflammation, development of necrotic granulomata, and a rapid death. Neutrophils act directly or indirectly on mycobacteria by different oxidative or other reactions including neutrophil extracellular traps (NETs) formation. Phagocytosis of mycobacteria by neutrophils is accompanied by the production of pro-inflammatory factors, thus making neutrophils active participants of inflammation in all stages of the infectious process. Finally, neutrophils die by apoptosis or necrosis. Necrosis of neutrophils, which is activated by reactive oxygen species, also prolongs the inflammation. In this way, there is strong evidence that neutrophils are the cells involved in the transition of infection to the terminal stage, participating in lung tissue destruction. Although neutrophils evolutionary developed many ways to resist pathogens, it is likely, that neutrophils do not possess sufficient anti-mycobactericidal capacities due to the development of many adaptations allowing mycobacteria to survive inside the neutrophils. Neutrophils effectively phagocytose but poorly kill mycobacteria, thus hiding bacilli from more efficient killers, macrophages, and playing the role of the “Trojan Horse”. In this review, we summarize the data on the involvement of neutrophils in TB inflammation. We discuss their ambiguous role in pathogenesis which depends upon mycobacterial virulence, host genetics, dynamics of migration to inflammatory foci, and persistence during initial and chronic stages of the infectious process.
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Prakash, Teron, Singh Kushwaha Rahul, and Tiwari |. Kaushal K. Chandrul Atul. "An Overview on Tuberculosis TB." International Journal of Trend in Scientific Research and Development 3, no. 3 (2019): 1820–25. https://doi.org/10.31142/ijtsrd23543.
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Tuberculosis TB stays one of the deadliest irresistible ailments in charge of millions of passing's every year over the world. In this paper we present a general review of TB including the pathogenesis, analysis, and treatment rules. In readiness of this review, we scanned PubMed for pertinent articles on TB. Furthermore, we looked through the sites of global establishments like the World Health Organization WHO and the US Centers for Disease control and Prevention CDC for related reports and clinical rules. This paper has been composed with the goal to offer general training to wellbeing experts, arrangement producers, patients and the general population. Prakash Teron | Rahul Singh Kushwaha | Atul Tiwari | Kaushal K. Chandrul "An Overview on Tuberculosis (TB)" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-3 | Issue-3 , April 2019, URL: https://www.ijtsrd.com/papers/ijtsrd23543.pdf
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Goletti, D., R. Pisapia, F. M. Fusco, A. Aiello, and R. Van Crevel. "Epidemiology, pathogenesis, clinical presentation and management of TB in patients with HIV and diabetes." International Journal of Tuberculosis and Lung Disease 27, no. 4 (2023): 284–90. http://dx.doi.org/10.5588/ijtld.22.0685.
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Caused by Mycobacterium tuberculosis, TB is the leading cause of death from an infectious disease. HIV and diabetes are recognised risk factors for progression of TB disease and both have a strong impact on the diagnosis and management of TB, threatening efforts to end TB globally. Here we provide the latest data on the complex interplay between these conditions. TB patients with HIV present systemic immune activation, increased HIV viral load, more severe clinical presentations and reduced success of TB therapy. Similarly, TB patients with diabetes are characterised by an exaggerated adaptive immunity, worsening of the clinical presentations and a higher risk for multidrug resistance and treatment failure. It is important to strengthen resources to prevent these comorbidities from occurring and to implement screening, early diagnosis and appropriate management strategies.
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Rudko, A. A., M. B. Freidin, Ye Yu Bragina, A. R. An, and V. P. Puzyryov. "SEARCH OF TUBERCULOSIS SUSCEPTIBILITY GENES USING THE RESULTS OF GENOME-WIDE ASSOCIATION STUDY OF CROHN’S DISEASE." Bulletin of Siberian Medicine 12, no. 3 (2013): 61–68. http://dx.doi.org/10.20538/1682-0363-2013-3-61-68.
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Crohn’s disease (CD) and tuberculosis (TB) share several mechanisms of pathogenesis, and this suggests they also have common genetic susceptibility factors. To test this hypothesis, we performed the analysis of association between TB and polymorphisms of genes associated with CD, according to the results of genome-wide association studies, in Russians from Tomsk and indigenous people from Tuva. For the first time, The rs2872507 (ORMDL3), rs3810936 (TNFSF15), rs10192702 (ATG16L1), rs9286879 (1q24.3), rs10507523 (13q14.11) polymorphisms were found to be associated with TB in Russians. The rs1407308 (TNFSF15) and rs1736135 (21q21.1) were associated with the disease in Tuvinians. The associations found are likely due to the functional role of the relevant proteins and their pathogenetic influence on the immune reaction underlying tuberculosis infection. Overall, the study of polymorphisms associated with CD allowed us to identify new candidate genes for TB.
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Pollara, Gabriele, Carolin T. Turner, Joshua Rosenheim, et al. "Exaggerated IL-17A activity in human in vivo recall responses discriminates active tuberculosis from latent infection and cured disease." Science Translational Medicine 13, no. 592 (2021): eabg7673. http://dx.doi.org/10.1126/scitranslmed.abg7673.
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Host immune responses at the site of Mycobacterium tuberculosis infection can mediate pathogenesis of tuberculosis (TB) and onward transmission of infection. We hypothesized that pathological immune responses would be enriched at the site of host-pathogen interactions modeled by a standardized tuberculin skin test (TST) challenge in patients with active TB compared to those without disease, and interrogated immune responses by genome-wide transcriptional profiling. We show exaggerated interleukin-17A (IL-17A) and T helper 17 (TH17) responses among 48 individuals with active TB compared to 191 with latent TB infection, associated with increased neutrophil recruitment and matrix metalloproteinase-1 expression, both involved in TB pathogenesis. Curative antimicrobial treatment reversed these observed changes. Increased IL-1β and IL-6 responses to mycobacterial stimulation were evident both in circulating monocytes and in molecular changes at the site of TST in individuals with active TB, supporting a model in which monocyte-derived IL-1β and IL-6 promote TH17 differentiation within tissues. Modulation of these cytokine pathways may provide a rational strategy for host-directed therapy in active TB.
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Kaushal, Deepak, Dhiraj K. Singh, and Smriti Mehra. "Immune Responses in Lung Granulomas during Mtb/HIV Co-Infection: Implications for Pathogenesis and Therapy." Pathogens 12, no. 9 (2023): 1120. http://dx.doi.org/10.3390/pathogens12091120.
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HIV and TB are the cause of significant worldwide mortality and pose a grave danger to the global public health. TB is the leading cause of death in HIV-infected persons, with one in four deaths attributable to TB. While the majority of healthy individuals infected with M. tuberculosis (Mtb) are able to control the infection, co-infection with HIV increases the risk of TB infection progressing to TB disease by over 20-fold. While antiretroviral therapy (ART), the cornerstone of HIV care, decreases the incidence of TB in HIV-uninfected people, this remains 4- to 7-fold higher after ART in HIV-co-infected individuals in TB-endemic settings, regardless of the duration of therapy. Thus, the immune control of Mtb infection in Mtb/HIV-co-infected individuals is not fully restored by ART. We do not fully understand the reasons why Mtb/HIV-co-infected individuals maintain a high susceptibility to the reactivation of LTBI, despite an effective viral control by ART. A deep understanding of the molecular mechanisms that govern HIV-induced reactivation of TB is essential to develop improved treatments and vaccines for the Mtb/HIV-co-infected population. We discuss potential strategies for the mitigation of the observed chronic immune activation in combination with both anti-TB and anti-retroviral approaches.
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Kulkarni, Smita, Janice J. Endsley, Zhao Lai, Todd Bradley, and Riti Sharan. "Single-Cell Transcriptomics of Mtb/HIV Co-Infection." Cells 12, no. 18 (2023): 2295. http://dx.doi.org/10.3390/cells12182295.
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Tuberculosis (TB) and Human Immunodeficiency Virus (HIV) co-infection continues to pose a significant healthcare burden. HIV co-infection during TB predisposes the host to the reactivation of latent TB infection (LTBI), worsening disease conditions and mortality. There is a lack of biomarkers of LTBI reactivation and/or immune-related transcriptional signatures to distinguish active TB from LTBI and predict TB reactivation upon HIV co-infection. Characterizing individual cells using next-generation sequencing-based technologies has facilitated novel biological discoveries about infectious diseases, including TB and HIV pathogenesis. Compared to the more conventional sequencing techniques that provide a bulk assessment, single-cell RNA sequencing (scRNA-seq) can reveal complex and new cell types and identify more high-resolution cellular heterogeneity. This review will summarize the progress made in defining the immune atlas of TB and HIV infections using scRNA-seq, including host-pathogen interactions, heterogeneity in HIV pathogenesis, and the animal models employed to model disease. This review will also address the tools needed to bridge the gap between disease outcomes in single infection vs. co-infection. Finally, it will elaborate on the translational benefits of single-cell sequencing in TB/HIV diagnosis in humans.
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Choudhury, Sreetama, Eliza Peterson, karolina Maciag, et al. "Identifying innate immune regulators of Mycobacterium tuberculosis pathogenesis in macrophages." Journal of Immunology 206, no. 1_Supplement (2021): 97.19. http://dx.doi.org/10.4049/jimmunol.206.supp.97.19.
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Abstract Tuberculosis (TB) is a leading infectious disease that contributes to approximately 1.4 million deaths annually worldwide. In the present situation of the COVID-19 pandemic and disrupted healthcare services, mathematical modelling predicts that there will be an additional 6.3 million new cases and 1.4 million more TB deaths by the end of 2025. Innate immune cells like macrophages are the frontline responders in host defense against Mycobacterium tuberculosis (MTB) and may also play a major role in disease establishment. A major roadblock in developing effective strategies against TB is the inability of current anti-TB drugs to target both replicating and non-replicating bacteria. We have found that lack of specific components of the host innate sensing machinery has a major impact on intracellular bacterial growth and the production of IL-1β and IFN-β during MTB infection of macrophages; the latter cytokines play major roles in host-protective and host-detrimental outcomes of infection respectively. RNA seq reveals that these innate immune modules differentially control the expression of genes implicated in host protein synthesis and MTB dissemination and escape from the granuloma. Ongoing work is utilizing Path-Seq for quantitative profiling of the MTB transcriptome within infected macrophages and investigating macrophage-dependent mechanisms of MTB restriction and persistence in vivo. Our study will potentially identify immune regulators that make the macrophage environment either permissive or restrictive for intracellular replication of MTB with important implications for developing combinatorial targeting approaches for host-directed treatment of TB.
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Biadglegne, Fantahun, Brigitte König, Arne C. Rodloff, Anca Dorhoi, and Ulrich Sack. "Composition and Clinical Significance of Exosomes in Tuberculosis: A Systematic Literature Review." Journal of Clinical Medicine 10, no. 1 (2021): 145. http://dx.doi.org/10.3390/jcm10010145.
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Tuberculosis (TB) remains a major health issue worldwide. In order to contain TB infections, improved vaccines as well as accurate and reliable diagnostic tools are desirable. Exosomes are employed for the diagnosis of various diseases. At present, research on exosomes in TB is still at the preliminary stage. Recent studies have described isolation and characterization of Mycobacterium tuberculosis (Mtb) derived exosomes in vivo and in vitro. Mtb-derived exosomes (Mtbexo) may be critical for TB pathogenesis by delivering mycobacterial-derived components to the recipient cells. Proteomic and transcriptomic analysis of Mtbexo have revealed a variety of proteins and miRNA, which are utilized by the TB bacteria for pathogenesis. Exosomes have been isolated in body fluids, are amenable for fast detection, and could contribute as diagnostic or prognostic biomarker to disease control. Extraction of exosomes from biological fluids is essential for the exosome research and requires careful standardization for TB. In this review, we summarized the different studies on Mtbexo molecules, including protein and miRNA and the methods used to detect exosomes in biological fluids and cell culture supernatants. Thus, the detection of Mtbexo molecules in biological fluids may have a potential to expedite the diagnosis of TB infection. Moreover, the analysis of Mtbexo may generate new aspects in vaccine development.
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Feldman, Charles, Annette J. Theron, Moloko C. Cholo, and Ronald Anderson. "Cigarette Smoking as a Risk Factor for Tuberculosis in Adults: Epidemiology and Aspects of Disease Pathogenesis." Pathogens 13, no. 2 (2024): 151. http://dx.doi.org/10.3390/pathogens13020151.
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It has been noted by the World Health Organisation that cases of tuberculosis in 2022 globally numbered 10.6 million, resulting in 1.3 million deaths, such that TB is one of the infectious diseases causing the greatest morbidity and mortality worldwide. Since as early as 1918, there has been an ongoing debate as to the relationship between cigarette smoking and TB. However, numerous epidemiological studies, as well as meta-analyses, have indicated that both active and passive smoking are independent risk factors for TB infection, development of reactivation TB, progression of primary TB, increased severity of cavitary disease, and death from TB, among several other considerations. With this considerable body of evidence confirming the association between smoking and TB, it is not surprising that TB control programmes represent a key potential preventative intervention. In addition to coverage of the epidemiology of TB and its compelling causative link with smoking, the current review is also focused on evidence derived from clinical- and laboratory-based studies of disease pathogenesis, most prominently the protective anti-mycobacterial mechanisms of the alveolar macrophage, the primary intracellular refuge of M. tuberculosis. This section of the review is followed by an overview of the major strategies utilised by the pathogen to subvert these antimicrobial mechanisms in the airway, which are intensified by the suppressive effects of smoke inhalation on alveolar macrophage function. Finally, consideration is given to a somewhat under-explored, pro-infective activity of cigarette smoking, namely augmentation of antibiotic resistance due to direct effects of smoke per se on the pathogen. These include biofilm formation, induction of cellular efflux pumps, which eliminate both smoke-derived toxicants and antibiotics, as well as gene modifications that underpin antibiotic resistance.
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Sankar, Poornima, Ramon Bossardi Ramos, Jamie Corro, et al. "Fatty acid metabolism in neutrophils promotes lung damage and bacterial replication during tuberculosis." PLOS Pathogens 20, no. 10 (2024): e1012188. http://dx.doi.org/10.1371/journal.ppat.1012188.
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Mycobacterium tuberculosis (Mtb) infection induces a marked influx of neutrophils into the lungs, which intensifies the severity of tuberculosis (TB). The metabolic state of neutrophils significantly influences their functional response during inflammation and interaction with bacterial pathogens. However, the effect of Mtb infection on neutrophil metabolism and its consequent role in TB pathogenesis remain unclear. In this study, we examined the contribution of glycolysis and fatty acid metabolism on neutrophil responses to Mtb HN878 infection using ex-vivo assays and murine infection models. We discover that blocking glycolysis aggravates TB pathology, whereas inhibiting fatty acid oxidation (FAO) yields protective outcomes, including reduced weight loss, immunopathology, and bacterial burden in lung. Intriguingly, FAO inhibition preferentially disrupts the recruitment of a pathogen-permissive immature neutrophil population (Ly6Glo/dim), known to accumulate during TB. Targeting carnitine palmitoyl transferase 1a (Cpt1a)-a crucial enzyme in mitochondrial β-oxidation-either through chemical or genetic methods impairs neutrophils’ ability to migrate to infection sites while also enhancing their antimicrobial function. Our findings illuminate the critical influence of neutrophil immunometabolism in TB pathogenesis, suggesting that manipulating fatty acid metabolism presents a novel avenue for host-directed TB therapies by modulating neutrophil functions.
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Todoriko, L. D., Y. I. Feshchenko, I. O. Semianiv, M. M. Kuzhko, O. S. Shevchenko, and R. L. Lyubevych. "ASPECTS OF CORONAVIRUS INFECTION PATHOGENESIS AND PROGNOSIS FOR PATHOMORPHOSIS OF PULMONARY TUBERCULOSIS DURING THE COVID-19 PANDEMIC." Ukrainian Pulmonology Journal 30, no. 2 (2022): 12–22. http://dx.doi.org/10.31215/2306-4927-2022-30-2-12-22.
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To date, the COVID-19 pandemic has surpassed all other health issues around the world. The interaction between COVID-19 and tuberculosis (TB), which remains the leading cause of death from a single infectious disease in the world, is important, as it can have serious consequences for both confirmed and underdiagnosed TB patients worldwide, especially in low- and middle-income countries, where TB is endemic and health services are poorly equipped. The aim of the study is to assess the prospects of the epidemiology of tuberculosis in the context of the COVID-19 pandemic and the consequences of the interaction between SARS-CoV-2 and Mycobacterium tuberculosis, taking into account the current situation in Ukraine. Materials and methods. Test access to various full-text and abstract databases was used. Results. Pathomorphological changes in COVID-19 patients are due to the direct action of SARS-CoV-2, hyperactivity of the immune system, high levels of cytotoxicity of CD8 + T cells, autoimmune processes. In view of all the above, the governments of TB-affected countries must ensure the continuity and effective provision of TB services during COVID-19. This includes the protection of the most vulnerable groups, including protection from economic hardship, isolation, stigma and discrimination. The global response should identify and mitigate potential risks to the TB-control mission. Conclusions. COVID-19 has pushed back anti-TB efforts for nearly a decade. This failure is likely to affect the long-term increase in TB morbidity and mortality worldwide. With low vaccination rates in TB-endemic countries and the emergence of new genotypes of the virus, this trend is likely to continue. Key words: COVID-19, tuberculosis, pathogenesis, treatment, epidemiology
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Anggraini, Debie. "The Role of Interleukin 10 Genetic Variations in Pulmonary Tuberculosis: Perspectives of Genetics, Pathogenesis and Immunology." Health and Medical Journal 6, no. 1 (2024): 68–79. http://dx.doi.org/10.33854/heme.v6i1.1487.
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Pulmonary tuberculosis remains a significant global public health challenge. In efforts to overcome this disease, a deeper understanding of the role of individual genetics, such as IL-10 genetic variation, in the response to M. tuberculosis infection is critical. Research that has been conducted shows that IL-10, which has an important role in regulating the immune response, can also influence the development of TB. Genetic variations in the IL-10 gene play a role in determining the extent of the immune response to TB infection and an individual's risk of this disease. The interaction between Treg cells, IL-10, and TB is also an important aspect in the pathogenesis and management of TB. Although Treg cells and IL-10 have a role in controlling excessive inflammation, too much of either can dampen the immune response needed to overcome infections. The implication of this research is that the development of more targeted and personalized therapy is an important step in overcoming TB. The use of individual genetic knowledge, such as IL-10 genetic variations, can help design more effective therapies and improve patient prognosis. However, challenges such as drug resistance and the complexity of genetic-immunological interactions remain challenges that need to be overcome in TB management. Overall, this study shows the importance of involving the fields of genetics and immunology in global efforts to address pulmonary tuberculosis. With a deeper understanding of the factors that influence the immune response to TB infection, we can hope to develop more effective strategies in the prevention, diagnosis and treatment of this disease and reduce the burden of TB worldwide.
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Riaz, Syeda Mariam, Kurt Hanevik, Lars Helgeland, Lisbet Sviland, Robert L. Hunter, and Tehmina Mustafa. "Novel Insights into the Pathogenesis of Human Post-Primary Tuberculosis from Archival Material of the Pre-Antibiotic Era, 1931–1947." Pathogens 12, no. 12 (2023): 1426. http://dx.doi.org/10.3390/pathogens12121426.
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Objectives: Primary and post-primary tuberculosis (TB) are distinct entities. The aim of this study was to study the histopathology of primary and post-primary TB by using the unique human autopsy material from the pre-antibiotic era, 1931–1947. Material and Methods: Autopsy data were collected from the autopsy journals, and the human tissue was collected from the pathology archives at the Department of Pathology, the Gades Institute. Results: Histological presentations of TB lesions showed great diversity within a single lung. Post-primary TB starts as a pneumonia forming early lesions, characterized by the infiltration of foamy macrophages containing mycobacterial antigens within alveoli, and progressing to necrotic pneumonias with an increasing density of mycobacterial antigens in the lesions. These necrotic pneumonic lesions appeared to either resolve as fibrocaseous lesions or lead to cavitation. The typical granulomatous inflammation, the hallmark of TB lesions, appeared later in the post-primary TB and surrounded the pneumonic lesions. These post-primary granulomas contained lesser mycobacterial antigens as compared to necrotic pneumonia. Conclusions: Immunopathogenesis of post-primary TB is different from primary TB and starts as pneumonia. The early lesions of post-primary TB may progress or regress, holding the key to understanding how a host can develop the disease despite an effective TB immunity.
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De Maio, Flavio, Flavia Squeglia, Delia Goletti, and Giovanni Delogu. "The Mycobacterial HBHA Protein: A Promising Biomarker for Tuberculosis." Current Medicinal Chemistry 26, no. 11 (2019): 2051–60. http://dx.doi.org/10.2174/0929867325666181029165805.
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A major goal in tuberculosis (TB) research is the identification, among the subjects infected with Mycobacterium tuberculosis (Mtb), of those with active TB, or at higher risk of developing active disease, from the latently infected subjects. The classical heterogeneity of Mtb infection and TB disease is a major obstacle toward the identification of reliable biomarkers that can stratify Mtb infected subjects based on disease risk. The heparin-binding haemagglutinin (HBHA) is a mycobacterial surface antigen that is implicated in tuberculosis (TB) pathogenesis. The host immune response against HBHA varies depending on the TB status and several studies are supporting the role of HBHA as a useful biomarker of TB.
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Smith, Issar. "Mycobacterium tuberculosis Pathogenesis and Molecular Determinants of Virulence." Clinical Microbiology Reviews 16, no. 3 (2003): 463–96. http://dx.doi.org/10.1128/cmr.16.3.463-496.2003.
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SUMMARY Tuberculosis (TB), one of the oldest known human diseases. is still is one of the major causes of mortality, since two million people die each year from this malady. TB has many manifestations, affecting bone, the central nervous system, and many other organ systems, but it is primarily a pulmonary disease that is initiated by the deposition of Mycobacterium tuberculosis, contained in aerosol droplets, onto lung alveolar surfaces. From this point, the progression of the disease can have several outcomes, determined largely by the response of the host immune system. The efficacy of this response is affected by intrinsic factors such as the genetics of the immune system as well as extrinsic factors, e.g., insults to the immune system and the nutritional and physiological state of the host. In addition, the pathogen may play a role in disease progression since some M. tuberculosis strains are reportedly more virulent than others, as defined by increased transmissibility as well as being associated with higher morbidity and mortality in infected individuals. Despite the widespread use of an attenuated live vaccine and several antibiotics, there is more TB than ever before, requiring new vaccines and drugs and more specific and rapid diagnostics. Researchers are utilizing information obtained from the complete sequence of the M. tuberculosis genome and from new genetic and physiological methods to identify targets in M. tuberculosis that will aid in the development of these sorely needed antitubercular agents.
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Arya, Rakesh, Hemlata Shakya, Viplov Kumar Biswas, et al. "Bioinformatics-Driven Identification of Ferroptosis-Related Gene Signatures Distinguishing Active and Latent Tuberculosis." Genes 16, no. 6 (2025): 716. https://doi.org/10.3390/genes16060716.
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Background: Tuberculosis (TB) remains a major global public health challenge, and diagnosing it can be difficult due to issues such as distinguishing active TB from latent TB infection (LTBI), as well as the sample collection process, which is often time-consuming and lacks sensitivity and specificity. Ferroptosis is emerging as an important factor in TB pathogenesis; however, its underlying molecular mechanisms are not fully understood. Thus, there is a critical need to establish ferroptosis-related diagnostic biomarkers for tuberculosis (TB). Methods: This study aimed to identify and validate potential ferroptosis-related genes in TB infection while enhancing clinical diagnostic accuracy through bioinformatics-driven gene identification. The microarray expression profile dataset GSE28623 from the Gene Expression Omnibus (GEO) database was used to identify ferroptosis-related differentially expressed genes (FR-DEGs) associated with TB. Subsequently, these genes were used for immune cell infiltration, Gene Set Enrichment Analysis (GSEA), functional enrichment and correlation analyses. Hub genes were identified using Weighted Gene Co-expression Network Analysis (WGCNA) and validated in independent datasets GSE37250, GSE39940, GSE19437, and GSE31348. Results: A total of 21 FR-DEGs were identified. Among them, four hub genes (ACSL1, PARP9, TLR4, and ATG3) were identified as diagnostic biomarkers. These biomarkers were enriched in immune-response related pathways and were validated. Immune cell infiltration, GSEA, functional enrichment and correlation analyses revealed that multiple immune cell types could be activated by FR-DEGs. Throughout anti-TB therapy, the expression of the four hub gene signatures significantly decreased in patients cured of TB. Conclusions: In conclusion, ferroptosis plays a key role in TB pathogenesis. These four hub gene signatures are linked with TB treatment effectiveness and show promise as biomarkers for differentiating TB from LTBI.
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Rabaan, Ali A., Saad Alhumaid, Hawra Albayat, et al. "Promising Antimycobacterial Activities of Flavonoids against Mycobacterium sp. Drug Targets: A Comprehensive Review." Molecules 27, no. 16 (2022): 5335. http://dx.doi.org/10.3390/molecules27165335.
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Tuberculosis (TB) caused by the bacterial pathogen Mycobacterium tuberculosis (Mtb) remains a threat to mankind, with over a billion of deaths in the last two centuries. Recent advancements in science have contributed to an understanding of Mtb pathogenesis and developed effective control tools, including effective drugs to control the global pandemic. However, the emergence of drug resistant Mtb strains has seriously affected the TB eradication program around the world. There is, therefore, an urgent need to develop new drugs for TB treatment, which has grown researchers’ interest in small molecule-based drug designing and development. The small molecules-based treatments hold significant potential to overcome drug resistance and even provide opportunities for multimodal therapy. In this context, various natural and synthetic flavonoids were reported for the effective treatment of TB. In this review, we have summarized the recent advancement in the understanding of Mtb pathogenesis and the importance of both natural and synthetic flavonoids against Mtb infection studied using in vitro and in silico methods. We have also included flavonoids that are able to inhibit the growth of non-tubercular mycobacterial organisms. Hence, understanding the therapeutic properties of flavonoids can be useful for the future treatment of TB.
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Drain, Paul K., Kristina L. Bajema, David Dowdy, et al. "Incipient and Subclinical Tuberculosis: a Clinical Review of Early Stages and Progression of Infection." Clinical Microbiology Reviews 31, no. 4 (2018): e00021-18. http://dx.doi.org/10.1128/cmr.00021-18.
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SUMMARY Tuberculosis (TB) is the leading infectious cause of mortality worldwide, due in part to a limited understanding of its clinical pathogenic spectrum of infection and disease. Historically, scientific research, diagnostic testing, and drug treatment have focused on addressing one of two disease states: latent TB infection or active TB disease. Recent research has clearly demonstrated that human TB infection, from latent infection to active disease, exists within a continuous spectrum of metabolic bacterial activity and antagonistic immunological responses. This revised understanding leads us to propose two additional clinical states: incipient and subclinical TB. The recognition of incipient and subclinical TB, which helps divide latent and active TB along the clinical disease spectrum, provides opportunities for the development of diagnostic and therapeutic interventions to prevent progression to active TB disease and transmission of TB bacilli. In this report, we review the current understanding of the pathogenesis, immunology, clinical epidemiology, diagnosis, treatment, and prevention of both incipient and subclinical TB, two emerging clinical states of an ancient bacterium.
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Goldfeld, Anne, and Jerrold J. Ellner. "Pathogenesis and management of HIV/TB co-infection in Asia." Tuberculosis 87 (August 2007): S26—S30. http://dx.doi.org/10.1016/j.tube.2007.05.003.
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Hancox, M. "Bovine TB in badgers: a reappraisal of aetiology and pathogenesis." Respiratory Medicine 90, no. 6 (1996): 371–73. http://dx.doi.org/10.1016/s0954-6111(96)90141-9.
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Oswal, Neelam, Hariprasad Thangavel, Kezia Lizardo, et al. "Diets Differently Regulate Pulmonary Pathogenesis and Immune Signaling in Mice during Acute and Chronic Mycobacterium tuberculosis Infection." Life 13, no. 1 (2023): 228. http://dx.doi.org/10.3390/life13010228.
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Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb) infection persists as a leading cause of mortality and morbidity globally, especially in developing and underdeveloped countries. The prevalence of TB-DM (diabetes mellitus) is higher in low- and middle-income countries where TB and DM are most prevalent. Epidemiological data suggest that slight obesity reduces the risk of TB, whereas DM increases the risk of pulmonary TB. Diets can alter the levels of body fat mass and body mass index by regulating systemic adiposity. Earlier, using a transgenic Mtb-infected murine model, we demonstrated that loss of body fat increased the risk of pulmonary bacterial load and pathology. In the present study, we investigated whether increased adiposity alters pulmonary pathology and bacterial load using C57BL/6 mice infected with HN878 Mtb strain and fed a medium-fat diet (MFD). We analyzed the effects of MFD on the lung during acute and chronic infections by comparing the results to those obtained with infected mice fed a regular diet (RD). Histological and biochemical analyses demonstrated that MFD reduces bacterial burden by increasing the activation of immune cells in the lungs during acute infection and reduces necrosis in the lungs during chronic infection by decreasing lipid accumulation. Our data suggest that slight adiposity likely protects the host during active TB infection by regulating immune and metabolic conditions in the lungs.
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Oehadian, Amaylia, Prayudi Santoso, Dick Menzies, and Rovina Ruslami. "Concise Clinical Review of Hematologic Toxicity of Linezolid in Multidrug-Resistant and Extensively Drug-Resistant Tuberculosis: Role of Mitochondria." Tuberculosis and Respiratory Diseases 85, no. 2 (2022): 111–21. http://dx.doi.org/10.4046/trd.2021.0122.
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Multidrug-resistant tuberculosis (MDR-TB) is caused by an organism that is resistant to both rifampicin and isoniazid. Extensively drug-resistant TB, a rare type of MDR-TB, is caused by an organism that is resistant to quinolone and one of group A TB drugs (i.e., linezolid and bedaquiline). In 2018, the World Health Organization revised the groupings of TB medicines and reclassified linezolid as a group A drug for the treatment of MDR-TB. Linezolid is a synthetic antimicrobial agent in the oxazolidinone class. Although linezolid has a good efficacy, it can cause substantial adverse events, especially hematologic toxicity. In both TB infection and linezolid mechanism of action, mitochondrial dysfunction plays an important role. In this concise review, characteristics of linezolid as an anti-TB drug are summarized, including its efficacy, pathogenesis of hematologic toxicity highlighting mitochondrial dysfunction, and the monitoring and management of hematologic toxicity.
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Ekaza, Euloge, Raymond Kouassi N’Guessan, Adèle Kacou-N’Douba, et al. "Emergence in Western African Countries of MDR-TB, Focus on Côte d’Ivoire." BioMed Research International 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/426709.
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Tuberculosis (TB) is responsible for a high mortality rate (2.5%) worldwide, mainly in developing countries with a high prevalence of human immunodeficiency virus (HIV). The emergence of multiresistant strains of TB poses an extreme risk for TB outbreaks and highlights the need for global TB control strategies. Among Western African countries, Côte d’Ivoire (CI) represents a specific example of a country with great potential to prevent TB. Specifically, CI has a promising healthcare system for monitoring diseases, including vaccination programs. However, military and political conflict in CI favors the spread of infectious diseases, TB being among the most devastating. Compilation of the studies identifying common causes of TB would be extremely beneficial for the development of treatment and prevention strategies. Therefore, the purpose of this comprehensive review is to evaluate the epidemiology of TB in CI, describe the factors involved in pathogenesis, and suggest simple and applicable prevention strategies.
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Salim Al-Karawi, Abdullah, Afraa Ali Kadhim, and Maha M. Kadum. "Recent advances in tuberculosis: A comprehensive review of emerging trends in pathogenesis, diagnostics, treatment, and prevention." International Journal of Clinical Biochemistry and Research 10, no. 4 (2024): 262–69. http://dx.doi.org/10.18231/j.ijcbr.2023.048.
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It is an in-depth analysis of a globally significant infectious disease, tuberculosis (TB). It covers the epidemiology, pathogenesis, diagnosis, treatment and prevention of TB with attention to its successes and shortcomings. The review examines this complicated relationship between Mycobacterium tuberculosis and the human host. It describes how outcomes move from latent infection to active disease. An Overview It introduces the current diagnostic methods, therapeutic regimens and preventive strategies; repeated emphasis is placed on targeted interventions and public health efforts. Also, the review covers future efforts in TB research and control that will further improve prevention and treatment. These include vaccines; new drugs (including a quest for novel agents); improved diagnostics (such as more rapid tests or smear-free methods); public health interventions such as policies on occupational exposures to respiratory rusts; integrated care models including continuity of services between Through these points the review illuminates how much can still be accomplished in terms of controlling--and even eliminating entirely--TB, with ramifications for global public health.
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Saxena, P., S. M. Kumar, and P. Pooja. "A study of an Incidence of tuberculosis is linked to elevated hepcidin at HIV diagnosis." CARDIOMETRY, no. 25 (February 14, 2023): 1441–43. http://dx.doi.org/10.18137/cardiometry.2022.25.14411443.
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Background: Hepcidin prevents ferroportin-mediated iron efflux, which results in intracellular macrophage iron retention and may encourage Mycobacterium tuberculosis nutrient absorption and TB pathogenesis. Aims & Objectives: In order to research into the relationship between incident pulmonary and extrapulmonary TB and plasma hepcidin levels, a retrospective cohort of HIV-positive, antiretroviral-native individuals had their plasma hepcidin levels tested at HIV diagnosis. Methods & Materials: Between 5 August 2017 and 1 June 2019, 140 individuals were monitored, and 34 incident TB cases were found. Discussion: After a median time to TB of 7 months, higher hepcidin was linked to a significantly increased chance of TB. Conclusion: The need for time-sensitive biomarkers that can detect individual variations in TB risk and the elucidation of iron-related causative pathways cannot be overstated.
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Azevedo-Pereira, José Miguel, David Pires, Marta Calado, Manoj Mandal, Quirina Santos-Costa, and Elsa Anes. "HIV/Mtb Co-Infection: From the Amplification of Disease Pathogenesis to an “Emerging Syndemic”." Microorganisms 11, no. 4 (2023): 853. http://dx.doi.org/10.3390/microorganisms11040853.
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Human immunodeficiency virus (HIV) and Mycobacterium tuberculosis (Mtb) are pathogens responsible for millions of new infections each year; together, they cause high morbidity and mortality worldwide. In addition, late-stage HIV infection increases the risk of developing tuberculosis (TB) by a factor of 20 in latently infected people, and even patients with controlled HIV infection on antiretroviral therapy (ART) have a fourfold increased risk of developing TB. Conversely, Mtb infection exacerbates HIV pathogenesis and increases the rate of AIDS progression. In this review, we discuss this reciprocal amplification of HIV/Mtb coinfection and how they influence each other’s pathogenesis. Elucidating the infectious cofactors that impact on pathogenesis may open doors for the design of new potential therapeutic strategies to control disease progression, especially in contexts where vaccines or the sterile clearance of pathogens are not effectively available.
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Roth, Andrew T., Jennifer A. Philips, and Pallavi Chandra. "The role of cholesterol and its oxidation products in tuberculosis pathogenesis." Immunometabolism 6, no. 2 (2024): e00042. http://dx.doi.org/10.1097/in9.0000000000000042.
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Mycobacterium tuberculosis causes tuberculosis (TB), one of the world’s most deadly infections. Lipids play an important role in M. tuberculosis pathogenesis. M. tuberculosis grows intracellularly within lipid-laden macrophages and extracellularly within the cholesterol-rich caseum of necrotic granulomas and pulmonary cavities. Evolved from soil saprophytes that are able to metabolize cholesterol from organic matter in the environment, M. tuberculosis inherited an extensive and highly conserved machinery to metabolize cholesterol. M. tuberculosis uses this machinery to degrade host cholesterol; the products of cholesterol degradation are incorporated into central carbon metabolism and used to generate cell envelope lipids, which play important roles in virulence. The host also modifies cholesterol by enzymatically oxidizing it to a variety of derivatives, collectively called oxysterols, which modulate cholesterol homeostasis and the immune response. Recently, we found that M. tuberculosis converts host cholesterol to an oxidized metabolite, cholestenone, that accumulates in the lungs of individuals with TB. M. tuberculosis encodes cholesterol-modifying enzymes, including a hydroxysteroid dehydrogenase, a putative cholesterol oxidase, and numerous cytochrome P450 monooxygenases. Here, we review what is known about cholesterol and its oxidation products in the pathogenesis of TB. We consider the possibility that the biological function of cholesterol metabolism by M. tuberculosis extends beyond a nutritional role.
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Sayyed, Shamabanu, Sriranjini A.S., Kamalnath Selvakumar, and Raghavendra L.S. Hallur. "Exploring Mycobacterium tuberculosis microarray data: Identification of interleukin (IL) as a key deregulated gene family for targeted therapy with phytochemicals." Biomedicine 43, no. 6 (2024): 1667–76. http://dx.doi.org/10.51248/.v43i6.3915.
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Introduction and Aim: The contemporary global health landscape is shadowed by the persistent menace of Mycobacterium tuberculosis, the etiological agent of tuberculosis (TB), a recalcitrant infectious malady. Despite medical advances, TB remains a formidable health threat, necessitating innovative strategies. Emerging drug-resistant strains further complicate its management, compelling the quest for novel biomarkers and therapeutic targets. In this context, biomarker identification assumes salience for enhanced TB management.
 
 Methods: The Microarray technology, with its multifaceted gene expression analysis capability, gains prominence in this endeavor. Employing microarray datasets, this study identified perturbed gene families, discerning nuanced TB pathogenesis and drug resistance through network pharmacology. In-silico computational techniques including molecular docking, molecular dynamic simulation and pharmacokinetics were employed to attain a comprehensive understanding of pharmacological attributes of phytocompounds towards interleukins.
 
 Results: Intriguingly, the representatives of the IL family were overrepresented and highly deregulated. To address TB's therapeutic conundrum, the study synthesizes microarray insights with phytochemical potential. Strikingly, IL-6 manifested as a key player, engaging in substantial protein-protein interactions within the network. Molecular docking unveiled Quercetin, Apigenin, Luteolin, Eupatilin, and Jaceidin as potent IL-6 interactors, with Quercetin showcasing notable binding affinity.
 .
 Conclusion: Quercetin, an anti-inflammatory agent, targeting IL-6 might mitigate detrimental immune responses and tissue damage, aiding TB management. Further exploration involves in vitro and in vivo validation of Quercetin-IL-6 interactions, assessing their impact on TB immune responses and pathogenesis. This study pioneers’ potential interventions, merging gene insights with phytochemical prowess, towards innovative TB management.
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Sanyal, Mousumi, F. Aaysha Cader, Muhammed Al Amin, Aparna Das, and M. Azizul Kahhar. "AIDS with Disseminated Tuberculosis." Journal of Bangladesh College of Physicians and Surgeons 34, no. 3 (2017): 168–71. http://dx.doi.org/10.3329/jbcps.v34i3.32351.
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Tuberculosis (TB) and Human Immunodeficiency Virus (HIV) have been closely linked since the emergence of the Acquired Immune Deficiency Syndrome(AIDS). Worldwide, TB is the most common opportunistic infection affecting HIV-seropositive individuals,and it remains the most common cause of death in patients with AIDS. By producing a progressive decline in cell-mediated immunity, HIV alters the pathogenesis of TB, greatly increasing the risk of disease from TB in HIV-coinfected individuals, and leading to more frequent extrapulmonary involvement, atypical radiographic manifestations, and paucibacillary disease, which can impede timely diagnosis. Although HIV-related TB is both treatable and preventable, incidence continues to climb in developing nations, wherein HIV infection and TB are endemic and resources are limited. We report the case of a 45 year old gentleman who presented with generalized lymphadenopathy, whose lymphnode biopsy was consistent with TB; however following poor response to anti-TB treatment, he was found to be serologically positive for HIV.J Bangladesh Coll Phys Surg 2016; 34(3): 168-171
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Dawi, John, Stephen Affa, Kevin Kafaja, et al. "The Role of Ferroptosis and Cuproptosis in Tuberculosis Pathogenesis: Implications for Therapeutic Strategies." Current Issues in Molecular Biology 47, no. 2 (2025): 99. https://doi.org/10.3390/cimb47020099.
Full textAbstract:
Tuberculosis (TB) caused by Mycobacterium tuberculosis (M.tb) remains a global health crisis, with over 10 million people affected annually. Despite advancements in treatment, M.tb has developed mechanisms to evade host immune responses, complicating efforts to eradicate the disease. Two emerging cell death pathways, ferroptosis and cuproptosis, have been linked to TB pathogenesis. Ferroptosis, an iron-dependent form of cell death, is driven by lipid peroxidation and reactive oxygen species (ROS) accumulation. This process can limit M.tb replication by depleting intracellular iron and inducing macrophage necrosis. However, excessive ferroptosis may lead to tissue damage and aid bacterial dissemination. Cuproptosis, triggered by copper accumulation, disrupts mitochondrial metabolism, leading to protein aggregation and cell death. M.tb exploits both iron and copper metabolism to survive within macrophages, manipulating these processes to resist oxidative stress and immune responses. This review examines the roles of ferroptosis and cuproptosis in TB, discussing how M.tb manipulates these pathways for survival. While therapeutic strategies targeting these processes, such as ferroptosis inducers (Erastin, RSL3) and inhibitors (Ferrostatin-1) and copper ionophores (Disulfiram, Elesclomol) and chelators, show promise, the limited understanding of these pathways and potential off-target effects remains a significant challenge. Further exploration of these pathways may provide insights into the development of targeted therapies aimed at controlling M.tb infection while minimizing host tissue damage. By elucidating the complex interactions between ferroptosis, cuproptosis, and TB, future therapies could better address bacterial resistance and improve clinical outcomes.
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Todoriko, L. D., Ya I. Toderika, O. S. Shevchenko, O. V. Pidverbetska, and O. Ya Pidverbetskyi. "The role of vitamin D deficiency in antituberculous protection." Infusion & Chemotherapy, no. 4 (December 27, 2021): 38–44. http://dx.doi.org/10.32902/2663-0338-2021-4-38-44.
Full textAbstract:
BACKGROUND. The main task of modern phthysiology is a comprehensive search for ways to optimize the etiotropic and the pathogenetic treatment of tuberculosis (TB). The search for improved treatment in addition to etiotropic antimicrobial therapy lies in the plane of improving pathogenetic therapy. Analysis of the available scientific sources suggests that the efficacy of TB treatment can be improved by adding vitamin D to the pathogenetic treatment, as vitamin D metabolites support the innate immune response to Mycobacterium tuberculosis.
 OBJECTIVE. To determine the role of vitamin D in the immunopathogenesis of the inflammatory response in pulmonary TB and to assess the prospects of its impact on improving the effectiveness of treatment by analyzing information from available scientific sources on this topic.
 MATERIALS AND METHODS. The study was performed for the period December 2020 – August 2021. The search was conducted by
 Keywords:
 pulmonary tuberculosis, vitamin D, mechanism of action, pathogenesis, treatment. Access to various full-text and abstract databases was used as the main source of research.
 RESULTS AND DISCUSSION. A large number of studies conducted so far prove the link between vitamin D deficiency and the occurrence of pulmonary TB. Vitamin D receptors have been found to be present on various surfaces of immune cells, including T and B cells, indicating that they need vitamin D to perform cellular functions. Vitamin D has been shown to increase the phagocytic activity of macrophages, and that monocytes incubated with cholecalciferol (vitamin D3) metabolites induce anti-TB activity. A number of studies have shown that vitamin D increases the body’s production of the antimicrobial/antimycobacterial peptide LL-37, a member of the cathelicidin petelide family. Therefore, the narrowly analyzed analysis according to the literature suggests that in the conditions of full vitamin D status of the human body the course of TB will be favorable, and in case of vitamin D deficiency – which is primarily associated with genetic polymorphisms, the course of TB may be unfavorable.
 CONCLUSIONS. Vitamin D functionates as one of the activators of macrophages and plays a role in the immune defense of the human body against mycobacterial TB. The inclusion of vitamin D in the program of complex treatment of TB infection is promising, as it enhances the production of antimicrobial/antimycobacterial peptide LL-37. It can be used as one of the components of TB prevention in children.