THE DIFFERENCE OF MAP1LC3 LEVEL AS MACROPHAGE AUTOPHAGY MARKER BETWEEN RESISTANT AND SENSITIVE TUBERCULOSIS PATIENTS ON RIFAMPICIN
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M. tuberculosis (MTB) is an intracelular bacteria that live in the host macrophage cells. Several organs can be affected by tuberculosis but most major illnesses are lung diseases. Immediately after infection, MTB will be phagocytosed by the alveolar macrophage cells and can survive in the phagosome. The macrophage plays a role in innate immunity towards an infection using autophagy by removing the microbe directly via phagocytosis. When bacteria phagocytosized, vacuole membrane formed double membranes called autophagosome, and followed by degradation by lysosome, which known as autolysosome. Induction of autophagy can be observed on the formation of microtubule-associated proteins 1B lightchain 3B (MAP1LC3B/LC3). MAP1LC3B is protein that have role at autophagic way for selection autophagy substrate and biogenesis. In this study we are used serum from patients TB with rifampicin resistant and rifampicin sensitive as control. Samples were divided using gene expert to differentiate between resistant and sensitive rifampicin.This research aims to compare MAP1LC3B levels in resistant and sensitive rifampicin to study macrophages respond in autophagic way in tuberculosis patients, and give information for define therapy plan to improve therapy for MDR-TB patients. Type of this research is a case control study design with cross sectional research with each groups sample is 19 from age 18-65 years old. Result, MAP1LC3B serum levels on the rifampicin resistant group are lower compared to rifampicin sensitive group. This occur because MTB is able to hide and evade innate immune defense mechanisms. MTB can maintain intracellular growth inside the phagosome by inhibiting phagolysosome formation in autophagy process especially inhibit MAP1LC3B formation by PDIM.
Patel DM, Patel SD, Jaiswal PS, Brahmbhatt KJ. Drug Resistant Mycobacterium tuberculosis and New Drug Development. Int J Drug Dev Res. 2012;4(2):76–91.
Lory S, DeLong EF, Thompson F, Stackebrandt E, Lory S, DeLong EF, et al. The Prokaryotes-Human Microbiology. Fourth Edi. New York: Springer Heidelberg; 2013.
Koch A, Mizrahi V, Warner DF. The impact of drug resistance on Mycobacterium tuberculosis physiology: what can we learn from rifampicin? Emerg Microbes Infect. 2014 Mar 12;3(3):e17–e17.
Boehme CC, Nabeta P, Hillemann D, Nicol MP, Shenai S, Krapp F, et al. Rapid Molecular Detection of Tuberculosis and Rifampin Resistance. N Engl J Med. 2010 Sep 9;363(11):1005–15.
Aziz MA, Wright A, Laszlo A, De Muynck A, Portaels F, Van Deun A, et al. Epidemiology of antituberculosis drug resistance (the Global Project on Anti-tuberculosis Drug Resistance Surveillance): an updated analysis. Lancet (London, England). 2006 Dec 16;368(9553):2142–54.
du Preez I, Loots DT. Altered fatty acid metabolism due to rifampicin-resistance conferring mutations in the rpoB Gene of Mycobacterium tuberculosis: mapping the potential of pharmaco-metabolomics for global health and personalized medicine. OMICS. 2012 Nov;16(11):596–603.
Gagneux S, Long CD, Small PM, Van T, Schoolnik GK, Bohannan BJM. The competitive cost of antibiotic resistance in Mycobacterium tuberculosis. Science. 2006 Jun 30;312(5782):1944–6.
Patel AS, Morse D, Choi AMK. Regulation and functional significance of autophagy in respiratory cell biology and disease. Am J Respir Cell Mol Biol. 2013 Jan;48(1):1–9.
Goletti D, Petruccioli E, Romagnoli A, Piacentini M, Fimia GM. Autophagy in Mycobacterium tuberculosis infection: a passepartout to flush the intruder out? Cytokine Growth Factor Rev. 2013 Aug;24(4):335–43.
Rosenberger CM, Finlay BB. Phagocyte sabotage: disruption of macrophage signalling by bacterial pathogens. Nat Rev Mol Cell Biol. 2003 May;4(5):385–96.
Kabeya Y, Mizushima N, Ueno T, Yamamoto A, Kirisako T, Noda T, et al. LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing. EMBO J. 2000 Nov 1;19(21):5720–8.
Gong L, Devenish RJ, Prescott M. Autophagy as a macrophage response to bacterial infection. IUBMB Life. 2012 Sep;64(9):740–7.
Flannagan RS, Heit B, Heinrichs DE. Antimicrobial Mechanisms of Macrophages and the Immune Evasion Strategies of Staphylococcus aureus. Pathog (Basel, Switzerland). 2015 Nov 27;4(4):826–68.
Bento CF, Empadinhas N, Mendes V. Autophagy in the fight against tuberculosis. DNA Cell Biol. 2015 Apr;34(4):228–42.
Podinovskaia M, Lee W, Caldwell S, Russell DG. Infection of macrophages with Mycobacterium tuberculosis induces global modifications to phagosomal function. Cell Microbiol. 2013 Jun;15(6):843–59.
Behar SM, Divangahi M, Remold HG. Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy? Nat Rev Microbiol. 2010;8(9):668–74.
Miskinyte M, Gordo I. Increased Survival of Antibiotic-Resistant Escherichia coli inside Macrophages. Antimicrob Agents Chemother. 2013 Jan;57(1):189–95.
Quigley J, Hughitt VK, Velikovsky CA, Mariuzza RA, El-Sayed NM, Briken V. The Cell Wall Lipid PDIM Contributes to Phagosomal Escape and Host Cell Exit of Mycobacterium tuberculosis. MBio. 2017 Mar 7;8(2).
Siegrist MS, Bertozzi CR. Mycobacterial lipid logic. Cell Host Microbe. 2014 Jan 15;15(1):1–2.
Astarie-Dequeker C, Le Guyader L, Malaga W, Seaphanh F-K, Chalut C, Lopez A, et al. Phthiocerol Dimycocerosates of M. tuberculosis Participate in Macrophage Invasion by Inducing Changes in the Organization of Plasma Membrane Lipids. Flynn JL, editor. PLoS Pathog. 2009 Feb 6;5(2):e1000289.
Comas I, Borrell S, Roetzer A, Rose G, Malla B, Kato-Maeda M, et al. Whole-genome sequencing of rifampicin-resistant Mycobacterium tuberculosis strains identifies compensatory mutations in RNA polymerase genes. Nat Genet. 2011 Dec 18;44(1):106–10.
Kawamura N, Kurokawa K, Ito T, Hamamoto H, Koyama H, Kaito C, et al. Participation of Rho-dependent transcription termination in oxidative stress sensitivity caused by an rpoB mutation. Genes Cells. 2005 May;10(5):477–87.
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