Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island

被引：941
作者：
Viala, J
Chaput, C
Boneca, IG
Cardona, A
Girardin, SE
Moran, AP
Athman, R
Mémet, S
Huerre, MR
Coyle, AJ
DiStefano, PS
Sansonetti, PJ
Labigne, A
Bertin, J
Philpott, DJ
Ferrero, RL
机构：
[1] Inst Pasteur, Grp Immun Innee & Signalisat, Paris, France
[2] Inst Pasteur, Unite Pathogenie Bacterienne Muqueuses, Paris, France
[3] Inst Pasteur, Unite Rech & Expertise Histotechnol & Pathol, Paris, France
[4] Inst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris, France
[5] Natl Univ Ireland, Dept Microbiol, Galway, Ireland
[6] Inst Pasteur, Unite Biol Mol Express Genique, Paris, France
[7] Millennium Pharmaceut Inc, Cambridge, MA USA
来源：
NATURE IMMUNOLOGY | 2004年 / 5卷 / 11期
关键词：
D O I：
10.1038/ni1131
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Epithelial cells can respond to conserved bacterial products that are internalized after either bacterial invasion or liposome treatment of cells. We report here that the noninvasive Gram-negative pathogen Helicobacter pylori was recognized by epithelial cells via Nod1, an intracellular pathogen-recognition molecule with specificity for Gram-negative peptidoglycan. Nod1 detection of H. pylori depended on the delivery of peptidoglycan to host cells by a bacterial type IV secretion system, encoded by the H. pylori cag pathogenicity island. Consistent with involvement of Nod1 in host defense, Nod1-deficient mice were more susceptible to infection by cag pathogenicity island-positive H. pylori than were wild-type mice. We propose that sensing of H. pylori by Nod1 represents a model for host recognition of noninvasive pathogens.
引用
收藏
页码：1166 / 1174
页数：9
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