pathogenesis of tuberculosis pdf levothroid

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Lipoarabinomannan, a major cell wall associated glycolipid, has been extensively examined in vitro and can inhibit gamma interferon activation of macrophages (Mycobacterial lipoarabinomannan inhibits gamma interferon-mediated activation of macrophages.Inhibition of interferon-gamma-mediated activation in mouse macrophages treated with lipoarabinomannan.Structural basis of capacity of lipoarabinomannan to induce secretion of tumor necrosis factor.Lipoarabinomannan, a possible virulence factor involved in persistence of Mycobacterium tuberculosis within macrophages.In vivo induction of apoptosis in the thymus by administration of mycobacterial cord factor (trehalose 6,6′-dimycolate).Cord factor (alpha,alpha-trehalose 6,6′-dimycolate) inhibits fusion between phospholipid vesicles.Phenolic glycolipid-I of Mycobacterium leprae induces general suppression of in vitro concanavalin A responses unrelated to leprosy type.Suppression of monocyte oxidative response by phenolic glycolipid I of Mycobacterium leprae.Role of the cell wall phenolic glycolipid-1 in the peripheral nerve predilection of Mycobacterium leprae.Using signature-tagged mutagenesis to screen for mycobacterial genes important for in vivo growth, two groups identified a cluster of Identification of a virulence gene cluster of Mycobacterium tuberculosis by signature-tagged transposon mutagenesis.Complex lipid determines tissue-specific replication of Mycobacterium tuberculosis in mice.Complex lipid determines tissue-specific replication of Mycobacterium tuberculosis in mice.Further evidence for the role of an individual lipid molecule in Oxygenated mycolic acids are necessary for virulence of mycobacterium tuberculosis in mice.Mycolic acids structure, biosynthesis and physiological functions.Oxygenated mycolic acids are necessary for virulence of mycobacterium tuberculosis in mice.Attenuation of virulence by disruption of the Mycobacterium tuberculosis erp gene.Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages.Expression of katG in Mycobacterium tuberculosis is associated with its growth and persistence in mice and guinea pigs.The glyoxylate shunt allows bacteria and plants to grow on acetate or fatty acids as sole carbon sources.




The other rabbit, who had shared the same conditions of life with the inoculated rabbit … did not show a single tubercle.” (Villimin had certainly established that tuberculosis was a transmissible disease, but he did not identify the causative agent. Extreme susceptibility to the disease has been observed in Eskimo populations in North America, in Yanomami Indians in the Brazilian Amazon, and in black populations in the United States (A clue to the genetic basis of resistance was provided by Gros and colleagues, who identified a strain of mice with exquisite vulnerability to overwhelming infection with leishmania, salmonella, and certain mycobacteria, particularly Several other genes and gene families, including those for vitamin D receptors and the components of IFN-γ–signaling pathways, have also been studied for their role in susceptibility to tuberculosis (Mycobacteria can be taken up by a variety of receptors on macrophages, including those for complement and surfactant, and as has been described more recently, through several of the toll-like receptors, including TLR2 and TLR4 (The granuloma is the cardinal feature of the initial host immune response to tuberculosis, and a great deal of effort has been devoted to understanding granuloma formation and its role in host defenses against Early insights into the formation and role of granulomas in tuberculosis pathogenesis were provided by the work of Lurie and Dannenberg, using a rabbit model, which has both advantages and disadvantages for making observations relevant to human disease (Recent work by Flynn and Chan has yielded several important insights into the role of granulomas in maintaining the latent state of tuberculosis infection, and has demonstrated the important role of the cytokine tumor necrosis factor-α (TNF-α) in maintaining granuloma function.

Infection occurs via aerosol, and inhalation of a few droplets containing M. tuberculosis bacilli.

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Using a murine model of latent infection in which mice inoculated via the tail vein with This work, demonstrating the critical role of TNF in maintaining granuloma structure and function in mice, has received striking confirmation in humans.



Pathologic manifestation of tuberculosis like caseating granuloma …






A twice-weekly, directly observed, and cost-effective regimen.Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence.Disseminated tuberculosis in interferon gamma gene-disrupted mice.Interleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with mycobacterium tuberculosis.Controlled clinical trial of four short-course (6 month) regimens of chemotherapy for treatment of pulmonary tuberculosis. The infection usually stays in the lungs.

Through the efforts of a tremendous number of dedicated investigators, many of the formidable technical obstacles to M. tuberculosis investigation have been surmounted such that rigorous analysis of M. tuberculosis pathogenesis is now possible.

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