|
Originally published In Press as doi:10.1074/jbc.M103831200 on June 18, 2001
J. Biol. Chem., Vol. 276, Issue 34, 32230-32239, August 24, 2001
Shigella Invasion of Macrophage
Requires the Insertion of IpaC into the Host Plasma Membrane
FUNCTIONAL ANALYSIS OF IpaC*
Asaomi
Kuwae,
Sei
Yoshida,
Koichi
Tamano,
Hitomi
Mimuro,
Toshihiko
Suzuki, and
Chihiro
Sasakawa
From the Department of Microbiology and Immunology, Institute of
Medical Science, University of Tokyo, 4-6-1 Shirokanedai,
Minato-ku, Tokyo 108-8639, Japan
Shigella infects residential
macrophages via the M cell entry, after which the pathogen induces
macrophage cell death. The bacterial strategy of macrophage infection,
however, remains largely speculative. Wild type Shigella
flexneri (YSH6000) invaded macrophages more efficiently than the
noninvasive mutants, where YSH6000 induced large scale lamellipodial
extension including ruffle formation around the bacteria. When
macrophages were infected with the noninvasive ipaC mutant,
the invasiveness and induction of membrane extension were dramatically
reduced as compared with that of YSH6000. J774 macrophages infected
with YSH6000 showed tyrosine phosphorylation of several proteins
including paxillin and c-Cbl, and this pattern was distinctive from
those stimulated by Salmonella typhimurium or phorbol
ester. Upon addition of IpaC into the external medium of macrophages,
membrane extensions were rapidly induced, and this promoted uptake of
Escherichia coli. The exogenously added IpaC was found to
be integrated into the host cell membrane as detected by
immunostaining. The IpaC domain required for the induction of membrane
extension from J774 was narrowed down within the region of residues
117-169, which contains a putative membrane-spanning sequence. Our
data indicate that Shigella directs its own entry into
macrophages, and the IpaC domain which is required for the association
with its host membrane is crucial.
*
This work was supported by the Research for the Future
Program of the Japan Society for the Promotion of Science and by Grant 11770135 from the Ministry of Education, Science, and Culture of the
Japanese Government.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.: 81-3-5449-5252;
Fax: 81-3-5449-5405; E-mail: sasakawa@ims.u-tokyo.ac.jp.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.

CiteULike Complore Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
G. N. Schroeder and H. Hilbi
Molecular Pathogenesis of Shigella spp.: Controlling Host Cell Signaling, Invasion, and Death by Type III Secretion
Clin. Microbiol. Rev.,
January 1, 2008;
21(1):
134 - 156.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
G. N. Schroeder, N. J. Jann, and H. Hilbi
Intracellular type III secretion by cytoplasmic Shigella flexneri promotes caspase-1-dependent macrophage cell death
Microbiology,
September 1, 2007;
153(9):
2862 - 2876.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A. Kuwae, T. Matsuzawa, N. Ishikawa, H. Abe, T. Nonaka, H. Fukuda, S. Imajoh-Ohmi, and A. Abe
BopC Is a Novel Type III Effector Secreted by Bordetella bronchiseptica and Has a Critical Role in Type III-dependent Necrotic Cell Death
J. Biol. Chem.,
March 10, 2006;
281(10):
6589 - 6600.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
T. Suzuki, K. Nakanishi, H. Tsutsui, H. Iwai, S. Akira, N. Inohara, M. Chamaillard, G. Nunez, and C. Sasakawa
A Novel Caspase-1/Toll-like Receptor 4-independent Pathway of Cell Death Induced by Cytosolic Shigella in Infected Macrophages
J. Biol. Chem.,
April 8, 2005;
280(14):
14042 - 14050.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
W. L. Picking, H. Nishioka, P. D. Hearn, M. A. Baxter, A. T. Harrington, A. Blocker, and W. D. Picking
IpaD of Shigella flexneri Is Independently Required for Regulation of Ipa Protein Secretion and Efficient Insertion of IpaB and IpaC into Host Membranes
Infect. Immun.,
March 1, 2005;
73(3):
1432 - 1440.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. Lucchini, H. Liu, Q. Jin, J. C. D. Hinton, and J. Yu
Transcriptional Adaptation of Shigella flexneri during Infection of Macrophages and Epithelial Cells: Insights into the Strategies of a Cytosolic Bacterial Pathogen
Infect. Immun.,
January 1, 2005;
73(1):
88 - 102.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
L. A. Kueltzo, J. Osiecki, J. Barker, W. L. Picking, B. Ersoy, W. D. Picking, and C. R. Middaugh
Structure-Function Analysis of Invasion Plasmid Antigen C (IpaC) from Shigella flexneri
J. Biol. Chem.,
January 24, 2003;
278(5):
2792 - 2798.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
L. J. Hathaway, G. E. Griffin, P. J. Sansonetti, and J. D. Edgeworth
Human Monocytes Kill Shigella flexneri but Then Die by Apoptosis Associated with Suppression of Proinflammatory Cytokine Production
Infect. Immun.,
July 1, 2002;
70(7):
3833 - 3842.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
T. Noda, H. Sagara, E. Suzuki, A. Takada, H. Kida, and Y. Kawaoka
Ebola Virus VP40 Drives the Formation of Virus-Like Filamentous Particles Along with GP
J. Virol.,
April 16, 2002;
76(10):
4855 - 4865.
[Abstract]
[Full Text]
[PDF]
|
 |
|
Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.
|
Advertisement
Advertisement
|