Document Detail


IglG and IglI of the Francisella pathogenicity island are important virulence determinants of Francisella tularensis LVS.
MedLine Citation:
PMID:  21690239     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The Gram-negative bacterium Francisella tularensis is the causative agent of tularemia, a disease intimately associated with the multiplication of the bacterium within host macrophages. This in turn requires the expression of Francisella pathogenicity island (FPI) genes, believed to encode a type VI secretion system. While the exact functions of many of the components have yet to be revealed, some have been found to contribute to the ability of Francisella to cause systemic infection in mice as well as to prevent phagolysosomal fusion and facilitate escape into the host cytosol. Upon reaching this compartment, the bacterium rapidly multiplies, inhibits activation of the inflammasome, and ultimately causes apoptosis of the host cell. In this study, we analyzed the contribution of the FPI-encoded proteins IglG, IglI, and PdpE to the aforementioned processes in F. tularensis LVS. The ΔpdpE mutant behaved similarly to the parental strain in all investigated assays. In contrast, ΔiglG and ΔiglI mutants, although they were efficiently replicating in J774A.1 cells, both exhibited delayed phagosomal escape, conferred a delayed activation of the inflammasome, and exhibited reduced cytopathogenicity as well as marked attenuation in the mouse model. Thus, IglG and IglI play key roles for modulation of the intracellular host response and also for the virulence of F. tularensis.
Authors:
Jeanette E Bröms; Moa Lavander; Lena Meyer; Anders Sjöstedt
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-06-20
Journal Detail:
Title:  Infection and immunity     Volume:  79     ISSN:  1098-5522     ISO Abbreviation:  Infect. Immun.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-08-17     Completed Date:  2011-10-21     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3683-96     Citation Subset:  IM    
Affiliation:
Department of Clinical Microbiology, Clinical Bacteriology, Umeå University, SE-901 85 Umeå, Sweden. jeanette.broms@climi.umu.se
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Bacterial Proteins / genetics
Bacterial Secretion Systems / genetics
Cell Line
Francisella tularensis / genetics*,  pathogenicity*
Gene Expression Regulation, Bacterial
Genes, Bacterial
Genomic Islands*
Inflammasomes / physiology
Macrophages / microbiology
Mice
Mice, Inbred C57BL
Microscopy, Electron, Transmission
Phagocytosis / genetics
Phagosomes / genetics,  metabolism,  microbiology
Polymerase Chain Reaction
Sequence Deletion
Tularemia / microbiology,  pathology
Virulence Factors / biosynthesis,  genetics*
Chemical
Reg. No./Substance:
0/Bacterial Proteins; 0/Inflammasomes; 0/Virulence Factors
Comments/Corrections

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


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