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结核分枝杆菌抑制吞噬体-溶酶体形成机制研究进展 被引量:1

Research Progress on mechanism of inhibition of phagosome-lysosome formation by Mycobacterium tuberculosis
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摘要 吞噬作用在机体对结核分枝杆菌进行降解、呈递、激活适应性免疫反应和清除病原的过程中不可或缺。在吞噬过程中,吞噬体囊泡发展成为成熟吞噬体需经过溶酶体融合、降低腔内pH值、酶的激活等一系列过程,并最终破坏吞噬微生物。单核细胞和巨噬细胞等吞噬细胞通过形成吞噬溶酶体参与宿主防御,而结核分枝杆菌表现出显著的阻断吞噬体成熟的能力,从而逃避宿主防御,并最终导致机体患病。本文就结核分枝杆菌抑制吞噬体-溶酶体形成机制的研究进展进行综述,以期为疾病的早期控制和新药的开发提供参考。 Phagocytosis is indispensable in the process of degradation,presentation,activation of adaptive immune response and clearance of Mycobacterium tuberculosis.In the process of phagocytosis,the development of phagosome vesicles into mature phagosomes requires a series of processes including lysosomal fusion,lowering the pH in the cavity,activation of enzymes,and finally destroying phagocytic microorganisms.Phagocytes,such as monocytes and macrophages,participate in host defense by forming phagolysosomes,while Mycobacterium tuberculosis exhibits a significant ability to block the maturation of phagosomes,thus escaping the host defenses and eventually leading to the disease.This article reviews the research progress on the mechanism of inhibition of phagocyte-lysosome formation by Mycobacterium tuberculosis,in order to provide a reference for the early control of disease and the development of new drugs.
作者 秦菱涔 杜先智 Qin Lingcen;Du Xianzhi(Department of Respiratory Medicine,the Second Affiliated Hospital,Chongqing Medical University,Chongqing 400010,China)
出处 《国际呼吸杂志》 2020年第3期211-214,共4页 International Journal of Respiration
基金 重庆市卫生计生委医学科研计划重点项目(2015ZDXM013)。
关键词 结核病 分枝杆菌 结核 吞噬体-溶酶体融合 Tuberculosis Mycobacterium tuberculosis Phagocyte-lysosome fusion
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  • 1Means T K,J Immunol,1999年,163卷,3920页
  • 2Dai G,Infect Immun,1998年,66卷,3562页
  • 3Flannagan RS, Cosio G, Grinstein S. Antimicrobial mechanisms of phagocytes and bacterial evasion strategies [J]. Nat Rev Microbiol, 2009,7(5) :355-366.
  • 4Mwandumba HC, Russell DG, Nyirenda MH, Anderson J, White SA, Molyneux ME, Squire SB. Mycobacterium tuberculosis resides in nonacidified vacuoles in endocytically competent alveolar macrophages from patients with tuberculosis and HIV infection [J]. J Immunol, 2004, 172 (7) : 4592-4598.
  • 5Hurtado-Lorenzo A, Skinner M, E1 Annan J, Futai M, Sun- Wada GH, Bourgoin S, Casanova J, Wildeman A, Bechoua S, Ausiello DA, Brown D, Marshansky V. V-ATPase interacts with ARNO and Arf6 in early endosomes and regulates the protein degradative pathway [J]. Nat Cell Biol, 2006,8(2) : 124-136.
  • 6Beyenbaeh KW, Wieczorek H. The V-type H+ ATPase: molecular structure and function, physiological roles and regulation [J]. J Exp Biol, 2006,209(Pt 4):577-589.
  • 7Via LE, Deretic D, Ulmer RJ, Hibler NS, Huber LA, Deretic V. Arrest of mycobacterial phagosome maturation is caused by a block in vesicle fusion between stages controlled by Rab5 and Rab7 [J]. J Biol Chem, 1997,272(20):13326- 13331.
  • 8Fratti RA, Backer JM, Gruenberg J, Corvera S, Deretic V. Role of phosphatidylinositol 3-kinase and Rab5 effectors in phagosomal biogenesis and mycobacterial phagosome maturation arrest [J]. J Cell Biol, 2001,154(3):631-644.
  • 9Sturgill-Koszycki S, Schlesinger PH, Chakraborty P, Haddix PL, Collins HL, Fok AK, Allen RD, Gluck SL, Heuser J, Russell DG. Lack of acidification in Mycobacterium phagosomes produced by exclusion of the vesicular proton-ATPase [J]. Science, 1994, 263 (5147): 678-681.
  • 10Wong D, Bach H, Sun J, Hmama Z, Av-Gay Y. Mycobacterium tuberculosis protein tyrosine phosphatase (PtpA) excludes host vacuolar-H+-ATPase to inhibit phagosome acidification [J]. Proc Natl Acad Sci USA, 2011,108(48) : 19371-19376.

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