Host-pathogen interactions Cell death and infection: A double-edged sword for host and pathogen survival

被引:268
作者
Ashida, Hiroshi [1 ]
Mimuro, Hitomi [1 ]
Ogawa, Michinaga [1 ]
Kobayashi, Taira [1 ]
Sanada, Takahito [2 ]
Kim, Minsoo [2 ]
Sasakawa, Chihiro [1 ,2 ]
机构
[1] Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan
[2] Univ Tokyo, Dept Infect Dis Control, Int Res Ctr Infect Dis, Inst Med Sci,Minato Ku, Tokyo 1088639, Japan
关键词
ENTEROPATHOGENIC ESCHERICHIA-COLI; ENTERICA SEROVAR TYPHIMURIUM; INNATE IMMUNE RECOGNITION; MYCOBACTERIUM-TUBERCULOSIS; KAPPA-B; EPITHELIAL-CELLS; MELANOMA; ANAPLASMA-PHAGOCYTOPHILUM; INFLAMMASOME ACTIVATION; FRANCISELLA-TULARENSIS;
D O I
10.1083/jcb.201108081
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Host cell death is an intrinsic immune defense mechanism in response to microbial infection. However, bacterial pathogens use many strategies to manipulate the host cell death and survival pathways to enhance their replication and survival. This manipulation is quite intricate, with pathogens often suppressing cell death to allow replication and then promoting it for dissemination. Frequently, these effects are exerted through modulation of the mitochondrial pro-death, NF-kappa B-dependent pro-survival, and inflammasome-dependent host cell death pathways during infection. Understanding the molecular details by which bacterial pathogens manipulate cell death pathways will provide insight into new therapeutic approaches to control infection.
引用
收藏
页码:931 / 942
页数:12
相关论文
共 102 条
[1]   Inflammasome-dependent Caspase-1 Activation in Cervical Epithelial Cells Stimulates Growth of the Intracellular Pathogen Chlamydia trachomatis [J].
Abdul-Sater, Ali A. ;
Koo, Evonne ;
Haecker, Georg ;
Ojcius, David M. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (39) :26789-26796
[2]   Anti-apoptotic signalling by the Dot/Icm secretion system of L-pneumophila [J].
Abu-Zant, Alaeddin ;
Jones, Snake ;
Asare, Rexford ;
Suttles, Jill ;
Price, Christopher ;
Graham, James ;
Abu Kwaik, Yousef .
CELLULAR MICROBIOLOGY, 2007, 9 (01) :246-264
[3]   Regulation of Legionella phagosome maturation and infection through flagellin and host Ipaf [J].
Amer, Amal ;
Franchi, Luigi ;
Kanneganti, Thirumala-Devi ;
Body-Malapel, Mathilde ;
Ozoren, Nesrin ;
Brady, Graham ;
Meshinchi, Sasha ;
Jagirdar, Rajesh ;
Gewirtz, Andrew ;
Akira, Shizuo ;
Nunez, Gabriel .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (46) :35217-35223
[4]   Host-bacterial interactions in Helicobacter pylori infection [J].
Amieva, Manuel R. ;
El-Omar, Emad M. .
GASTROENTEROLOGY, 2008, 134 (01) :306-323
[5]   The role of mitochondria in cellular defense against microbial infection [J].
Arnoult, Damien ;
Carneiro, Leticia ;
Tattoli, Ivan ;
Girardin, Stephen E. .
SEMINARS IN IMMUNOLOGY, 2009, 21 (04) :223-232
[6]   Legionella pneumophila inhibits macrophage apoptosis by targeting pro-death members of the Bcl2 protein family [J].
Banga, Simran ;
Gao, Ping ;
Shen, Xihui ;
Fiscus, Valena ;
Zong, Wei-Xing ;
Chen, Lingling ;
Luo, Zhao-Qing .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (12) :5121-5126
[7]   Temporal resolution of two-tracked NF-κB activation by Legionella pneumophila [J].
Bartfeld, Sina ;
Engels, Cecilia ;
Bauer, Bianca ;
Aurass, Philipp ;
Flieger, Antje ;
Brueggemann, Holger ;
Meyer, Thomas F. .
CELLULAR MICROBIOLOGY, 2009, 11 (11) :1638-1651
[8]   Metalloprotease type III effectors that specifically cleave JNK and NF-κB [J].
Baruch, Kobi ;
Gur-Arie, Lihi ;
Nadler, Chen ;
Koby, Simi ;
Yerushalmi, Gal ;
Ben-Neriah, Yinon ;
Yogev, Orli ;
Shaulian, Eitan ;
Guttman, Chen ;
Zarivach, Raz ;
Rosenshine, Ilan .
EMBO JOURNAL, 2011, 30 (01) :221-231
[9]   Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy? [J].
Behar, Samuel M. ;
Divangahi, Maziar ;
Remold, Heinz G. .
NATURE REVIEWS MICROBIOLOGY, 2010, 8 (09) :668-674
[10]   Macrophage activation redirects Yersinia-infected host cell death from apoptosis to caspase-1-dependent pyroptosis [J].
Bergsbaken, Tessa ;
Cookson, Brad T. .
PLOS PATHOGENS, 2007, 3 (11) :1570-1582