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牙龈卟啉单胞菌与细胞自噬相互作用研究进展 被引量:2

Research Progress in the Interaction between Porphyromonas gingivalis and Cell Autophagy
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摘要 细菌侵入细胞后转入自噬小体是细菌躲避宿主细胞的降解,引发自噬逃逸的一种重要途径。牙龈卟啉单胞菌(Porphyromonas gingivalis,Pg)是引起牙周炎和食管炎的重要致病菌。Pg侵入细胞后,通过对内源性转运以及自噬过程的修饰调节,使得内源性转运或自噬过程无法正常进行,从而逃逸宿主细胞的降解作用,同时在被修饰后的自噬小体中创造一个适宜细菌定植、增殖的微环境。本文综述Pg自噬逃逸、定植增殖过程的生物化学和形态学特征,分析Pg胞内定植增殖的机制。 That the bacteria transform into autophagosomes after their invading the cells is an important way for them to avoid degradation of host cells and induce autophagy escape.Porphyromonas gingivalis(Pg)is an important pathogen causing periodontitis and esophagitis.After the Pg invades the cells,the endogenous transport or autophagy process cannot be carried out normally through endogenous transport and modifying the regulation of autophagy process,so,the Pg could escape the degradation of host cells,and create a microenvironment suitable for their colonization and proliferation in the modified autophagosome.This paper reviews the biochemical and morphological characteristics of Pg autophagy escape,colonization and proliferation,and analyzes the mechanism of Pg intracellular colonization and proliferation.
作者 郭艺博 刘怡文 孙蔚 张秀森 孙玲云 张顶彧 原翔 高社干 GUO Yi-bo;LIU Yi-wen;SUN Wei;ZHANG Xiu-sen;SUN Ling-yun;ZHANG Ding-yu;YUAN Xiang;GAO She-gan(College of Clinical Medicine,The First Affiliated Hospital of Henan University of Science and Technology,Henan Key Laboratory of Cancer Epigenetics,Luoyang 471003,China)
出处 《食管疾病》 2020年第4期279-284,共6页 Journal of Esophageal Diseases
关键词 牙龈卟啉单胞菌 吞噬小体 自噬小体 自噬溶酶体 自噬逃逸 Porphyromonas gingivalis phagosome autophagosome autolysosome autophagy escape
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  • 1许良中,杨文涛.免疫组织化学反应结果的判断标准[J].中国癌症杂志,1996,6(4):229-231. 被引量:1365
  • 2Birmingham death by CL, Higgins autophagy : DE, Brumell interactions JH. Avoiding of Listeria monocytogenes with the macrophage autophagy system [J]. Autophagy,2008,4(3) : 368-371.
  • 3Py BF,Lipinski MM, Yuan J. Autophagy limits Listeria monocytogenes intracellular growth in the early phase of primary infection. Autophagy ,2007,3 (2) : 117-125.
  • 4Birmingham CL, Canadien V, Gouin E, et al. Listeria monocytogenes evades killing by autophagy during colonization of host cells [ J ]. Autophagy, 2007,3 (5) : 442-451.
  • 5Rodrigues PH, Belanger M, Dunn WJ Jr, et al. Porphyrornonas gingivalis and the autophagic pathway: an innate immune interaction [ J ] .? Front Biosci, 2008, 13 : 178-187.
  • 6Ogawa M, Yoshimori T, Suzuki T, et al. Escape of intracellular Shigella from autophagy [ J ] . Science, 2005,307(10) : 727-731.
  • 7Gutierrez MG, Master SS, Singh SB,et al. Autophagy is a defense mechanism inhibiting BCG and Mycobacterium tuberculosis survival in infected macrophages [ J ]. Cell, 2004,119(6) : 753-766.
  • 8Schmid D, Munz C. Innate and adaptive immunity through autophagy [ J ]. Immunity,2007,27 ( 1 ) : 2-11.
  • 9Paludan C, Schmid D, Landthaler M, et al. Endogenous MHC class Ⅱ processing of a viral nuclear antigen after autophagy [ J ]. Science, 2005,307 ( 5709 ) :593-596.
  • 10Harris J , De Haro SA , Master SS , et al. T helper 2 cytokines inhibit autophagic control of intracellular Mycobacterium tuberculosis [ J ]. Immunity ,2007,27 (3) : 505-517.

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