Host cell processes that influence the intracellular survival of Legionella pneumophila

被引:131
作者
Shin, Sunny [1 ]
Roy, Craig R. [1 ]
机构
[1] Yale Univ, Sch Med, Sect Microbial Pathogenesis, New Haven, CT 06536 USA
关键词
D O I
10.1111/j.1462-5822.2008.01145.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Key to the pathogenesis of intracellular pathogens is their ability to manipulate host cell processes, permitting the establishment of an intracellular replicative niche. In turn, the host cell deploys defence mechanisms that limit intracellular infection. The bacterial pathogen Legionella pneumophila, the aetiological agent of Legionnaire's Disease, has evolved virulence mechanisms that allow it to replicate within protozoa, its natural host. Many of these tactics also enable L. pneumophila's survival and replication inside macrophages within a membrane-bound compartment known as the Legionella-containing vacuole. One of the virulence factors indispensable for L. pneumophila's intracellular survival is a type IV secretion system, which translocates a large repertoire of bacterial effectors into the host cell. These effectors modulate multiple host cell processes and in particular, redirect trafficking of the L. pneumophila phagosome and mediate its conversion into an ER-derived organelle competent for intracellular bacterial replication. In this review, we discuss how L. pneumophila manipulates host cells, as well as host cell processes that either facilitate or impede its intracellular survival.
引用
收藏
页码:1209 / 1220
页数:12
相关论文
共 118 条
[61]   Legionella phagosomes intercept vesicular traffic from endoplasmic reticulum exit sites [J].
Kagan, JC ;
Roy, CR .
NATURE CELL BIOLOGY, 2002, 4 (12) :945-954
[62]   PONTIAC FEVER - ISOLATION OF THE ETIOLOGIC AGENT (LEGIONELLA-PNEUMOPHILA) AND DEMONSTRATION OF ITS MODE OF TRANSMISSION [J].
KAUFMANN, AF ;
MCDADE, JE ;
PATTON, CM ;
BENNETT, JV ;
SKALIY, P ;
FEELEY, JC ;
ANDERSON, DC ;
POTTER, ME ;
NEWHOUSE, VF ;
GREGG, MB ;
BRACHMAN, PS .
AMERICAN JOURNAL OF EPIDEMIOLOGY, 1981, 114 (03) :337-347
[63]   Phagocytosis of wild-type Legionella pneumophila occurs through a wortmannin-insensitive pathway [J].
Khelef, N ;
Shuman, HA ;
Maxfield, FR .
INFECTION AND IMMUNITY, 2001, 69 (08) :5157-5161
[64]   Evidence for pore-forming ability by Legionella pneumophila [J].
Kirby, JE ;
Vogel, JP ;
Andrews, HL ;
Isberg, RR .
MOLECULAR MICROBIOLOGY, 1998, 27 (02) :323-336
[65]   Legionella translocates an E3 ubiquitin ligase that has multiple U-boxes with distinct functions [J].
Kubori, Tomoko ;
Hyakutake, Akihiro ;
Nagai, Hiroki .
MOLECULAR MICROBIOLOGY, 2008, 67 (06) :1307-1319
[66]   A Legionella pneumophila-translocated substrate that is required for growth within macrophages and protection from host cell death [J].
Laguna, Rita K. ;
Creasey, Elizabeth A. ;
Li, Zhiru ;
Valtz, Nicole ;
Isberg, Ralph R. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (49) :18745-18750
[67]   The Nod-like receptor family member Naip5/Birc1e restricts Legionella pneumophila growth independently of caspase-1 activation [J].
Lamkanfi, Mohamed ;
Amer, Amal ;
Kanneganti, Thirumala-Devi ;
Munoz-Planillo, Ral ;
Chen, Grace ;
Vandenabeele, Peter ;
Fortier, Anne ;
Gros, Philippe ;
Nunez, Gabriel .
JOURNAL OF IMMUNOLOGY, 2007, 178 (12) :8022-8027
[68]   The prepilin peptidase is required for protein secretion by and the virulence of the intracellular pathogen Legionella pneumophila [J].
Liles, MR ;
Edelstein, PH ;
Cianciotto, NP .
MOLECULAR MICROBIOLOGY, 1999, 31 (03) :959-970
[69]   The Legionella pneumophila effector SidJ is required for efficient recruitment of endoplasmic reticulum proteins to the bacterial phagosome [J].
Liu, Yancheng ;
Luo, Zhao-Qing .
INFECTION AND IMMUNITY, 2007, 75 (02) :592-603
[70]   NF-κB translocation prevents host cell death after low-dose challenge by Legionella pneumophila [J].
Losick, Vicki P. ;
Isberg, Ralph R. .
JOURNAL OF EXPERIMENTAL MEDICINE, 2006, 203 (09) :2177-2189