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Tb Research Paper

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TB infection occurs through inhalation of Mtb containing airborne droplets dispersed from a TB infected person by coughing or sneezing. When the inhaled droplets reach the alveolar region of the lungs, the Mtb is quickly phagocytized by alveolar macrophages and other phagocytic cells, including neutrophils, monocyte-derived macrophages and dendritic cells [4]. The phagocytic cells most often kill the entered Mtb by phagosome-lysosome fusion. However, Mtb can inhibit the phagosome-lysosome fusion by blocking V-ATPase expression and increasing the accumulation of tryptophan-aspartate-containing coat protein around the phagosome membrane [5-7]. In addition, by generation of catalases, peroxidases and superoxide dismutases, Mtbs become resistant to macrophage attack, which allows them to persist in the macrophages.…show more content…
This multiplication continues until cell-mediated immune response developed. Once the adaptive cell-mediated immune response developed, migration of neutrophils, lymphocytes and other immune cells to the site of primary infection form a cellular infiltrate which is called granuloma [8]. The process takes approximately 2 years [9-11]. Granuloma is covered by fibrotic components, which becomes calcified where Mtb remains encapsulated inside and protected by the host immune response. The Mtb can survive for years, decades or for lifetime in this protective and non-metabolically active state (latent TB) [12]. During latent state, a dynamic equilibrium between Mtb and host immune response is established and any suitable conditions that weakens cell mediated immunity may lead to break down of granuloma, replication of bacteria and turn to active disease (active
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