| A comprehensive study of the contribution of Salmonella enterica serovar Typhimurium SPI2 effectors to bacterial colonization, survival, and replication in typhoid fever, macrophage, and epithelial cell infection models. | |
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MedLine Citation:
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PMID: 21540636 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Salmonella enterica serovars are Gram-negative bacterial pathogens responsible for human diseases including gastroenteritis and typhoid fever. After ingestion, Salmonella cross the intestinal epithelial barrier, where they are phagocytosed by macrophages and dendritic cells, which then enables their spread to systemic sites during cases of typhoid fever. Salmonella use two type 3 secretion systems encoded by Salmonella pathogenicity islands (SPI) 1 and 2 to inject virulence proteins into host cells to modify cellular functions. SPI1 is involved in host cell invasion and inflammation, whereas SPI2 is required for intracellular survival and replication within phagocytes, and systemic spread. In this study the contribution of nearly all known SPI2 effectors was examined in an in vivo model of murine typhoid fever and cell culture models of macrophage and epithelial cell infection. Unmarked, in-frame deletions of SPI2 effectors were engineered in S. enterica serovar Typhimurium and the ability of the 16 different mutants to colonize and replicate was examined. In the typhoid model, we found that ΔspvB and ΔspiC mutants were attenuated for colonization of intestinal and systemic sites, while the ΔsseF mutant was attenuated in systemic organs. In epithelial cells, all mutants replicated to the same extent as the wild-type. In macrophages, ΔspiC, ΔsteC, ΔspvB, ΔssseK1/K2/K3, ΔsifA, and ΔsifB strains replicated poorly in comparison to wild-type Salmonella. This study provides a thorough screen of the majority of the known SPI2 effectors evaluated under the same conditions in various models of infection, providing a foundation for comparative examination of the roles and interactions of these effectors. |
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Authors:
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Michelle M C Buckner; Matthew A Croxen; Ellen T Arena; B Brett Finlay |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-05-01 |
Journal Detail:
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Title: Virulence Volume: 2 ISSN: 2150-5608 ISO Abbreviation: Virulence Publication Date: 2011 May-Jun |
Date Detail:
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Created Date: 2011-06-30 Completed Date: 2011-10-19 Revised Date: 2012-05-01 |
Medline Journal Info:
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Nlm Unique ID: 101531386 Medline TA: Virulence Country: United States |
Other Details:
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Languages: eng Pagination: 208-16 Citation Subset: IM |
Affiliation:
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Department of Microbiology and Immunology and Michael Smith Laboratories, University of British Columbia, Canada. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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ADP Ribose Transferases
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genetics Animal Structures / microbiology Animals Bacterial Proteins / genetics Cell Line Disease Models, Animal Epithelial Cells / microbiology* Gene Deletion Genomic Islands* Humans Macrophages / microbiology* Mice Mice, Inbred C57BL Microbial Viability Salmonella Infections / microbiology* Salmonella typhimurium / genetics, growth & development, pathogenicity* Virulence Virulence Factors / genetics, metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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//Canadian Institutes of Health Research; //Howard Hughes Medical Institute |
| Chemical | |
Reg. No./Substance:
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0/Bacterial Proteins; 0/SpiC protein, Salmonella; 0/Virulence Factors; EC 2.4.2.-/ADP Ribose Transferases; EC 2.4.2.-/spvB protein, Salmonella enterica virulence plasmid |
| Comments/Corrections | |
Comment In:
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Virulence. 2011 May-Jun;2(3):177-80
[PMID:
21623168
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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