Document Detail


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.
MedLine Citation:
PMID:  21540636     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Michelle M C Buckner; Matthew A Croxen; Ellen T Arena; B Brett Finlay
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-05-01
Journal Detail:
Title:  Virulence     Volume:  2     ISSN:  2150-5608     ISO Abbreviation:  Virulence     Publication Date:    2011 May-Jun
Date Detail:
Created Date:  2011-06-30     Completed Date:  2011-10-19     Revised Date:  2012-05-01    
Medline Journal Info:
Nlm Unique ID:  101531386     Medline TA:  Virulence     Country:  United States    
Other Details:
Languages:  eng     Pagination:  208-16     Citation Subset:  IM    
Affiliation:
Department of Microbiology and Immunology and Michael Smith Laboratories, University of British Columbia, Canada.
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MeSH Terms
Descriptor/Qualifier:
ADP Ribose Transferases / 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:
//Canadian Institutes of Health Research; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
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:
Virulence. 2011 May-Jun;2(3):177-80   [PMID:  21623168 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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