Characterization of mediators of microbial virulence and innate immunity using the Caenorhabditis elegans host-pathogen model

被引:90
作者
Alegado, RA
Campbell, MC
Chen, WC
Slutz, SS
Tan, MW [1 ]
机构
[1] Stanford Univ, Dept Microbiol & Immunol, Sch Med, Stanford, CA 94305 USA
[2] Stanford Univ, Dept Genet, Sch Med, Stanford, CA 94305 USA
关键词
D O I
10.1046/j.1462-5822.2003.00287.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The soil-borne nematode, Caenorhabditis elegans , is emerging as a versatile model in which to study host-pathogen interactions. The worm model has shown to be particularly effective in elucidating both microbial and animal genes involved in toxin-mediated killing. In addition, recent work on worm infection by a variety of bacterial pathogens has shown that a number of virulence regulatory genes mediate worm susceptibility. Many of these regulatory genes, including the PhoP/Q two-component regulators in Salmonella and LasR in Pseudomonas aeruginosa , have also been implicated in mammalian models suggesting that findings in the worm model will be relevant to other systems. In keeping with this concept, experiments aimed at identifying host innate immunity genes have also implicated pathways that have been suggested to play a role in plants and animals, such as the p38 MAP kinase pathway. Despite rapid forward progress using this model, much work remains to be done including the design of more sensitive methods to find effector molecules and further characterization of the exact interaction between invading pathogens and C. elegans' cellular components.
引用
收藏
页码:435 / 444
页数:10
相关论文
共 56 条
[1]   Salmonella typhimurium proliferates and establishes a persistent infection in the intestine of Caenorhabditis elegans [J].
Aballay, A ;
Yorgey, P ;
Ausubel, FM .
CURRENT BIOLOGY, 2000, 10 (23) :1539-1542
[2]   Programmed cell death mediated by ced-3 and ced-4 protects Caenorhabditis elegans from Salmonella typhimurium-mediated killing [J].
Aballay, A ;
Ausubel, FM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (05) :2735-2739
[3]   Caenorhabditis elegans as a host for the study of host-pathogen interactions [J].
Aballay, A ;
Ausubel, FM .
CURRENT OPINION IN MICROBIOLOGY, 2002, 5 (01) :97-101
[4]   Caenorhabditis elegans innate immune response triggered by Salmonella enterica requires intact LPS and is mediated by a MAPK signaling pathway [J].
Aballay, A ;
Drenkard, E ;
Hilbun, LR ;
Ausubel, FM .
CURRENT BIOLOGY, 2003, 13 (01) :47-52
[5]  
[Anonymous], 1997, C ELEGANS
[6]   MAP kinase signalling cascade in Arabidopsis innate immunity [J].
Asai, T ;
Tena, G ;
Plotnikova, J ;
Willmann, MR ;
Chiu, WL ;
Gomez-Gomez, L ;
Boller, T ;
Ausubel, FM ;
Sheen, J .
NATURE, 2002, 415 (6875) :977-983
[7]  
BRENNER S, 1974, GENETICS, V77, P71
[8]   NF-κB family of transcription factors:: Central regulators of innate and adaptive immune functions [J].
Caamaño, J ;
Hunter, CA .
CLINICAL MICROBIOLOGY REVIEWS, 2002, 15 (03) :414-+
[9]   Diverse bacteria are pathogens of Caenorhabditis elegans [J].
Couillault, C ;
Ewbank, JJ .
INFECTION AND IMMUNITY, 2002, 70 (08) :4705-4707
[10]   Lethal paralysis of Caenorhabditis elegans by Pseudomonas aeruginosa [J].
Darby, C ;
Cosma, CL ;
Thomas, JH ;
Manoil, C .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (26) :15202-15207