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Host-pathogen interactions Cell death and infection: A double-edged sword for host and pathogen survival
被引:268
作者:

Ashida, Hiroshi
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Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan

Mimuro, Hitomi
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Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan

Ogawa, Michinaga
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Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan

Kobayashi, Taira
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Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan

Sanada, Takahito
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机构:
Univ Tokyo, Dept Infect Dis Control, Int Res Ctr Infect Dis, Inst Med Sci,Minato Ku, Tokyo 1088639, Japan Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan

Kim, Minsoo
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机构:
Univ Tokyo, Dept Infect Dis Control, Int Res Ctr Infect Dis, Inst Med Sci,Minato Ku, Tokyo 1088639, Japan Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan

Sasakawa, Chihiro
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机构:
Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan
Univ Tokyo, Dept Infect Dis Control, Int Res Ctr Infect Dis, Inst Med Sci,Minato Ku, Tokyo 1088639, Japan Univ Tokyo, Dept Microbiol & Immunol, Minato Ku, Tokyo 1088639, Japan
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.
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页码:931 / 942
页数:12
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