id:"swepub:oai:DiVA.org:umu-83830"
Search: id:"swepub:oai:DiVA.org:umu-83830" > IglG and IglI of th...
- 1 of 1
- Previous record
- Next record
- To hitlist
IglG and IglI of the Francisella pathogenicity island are important virulence determinants of Francisella tularensis LVS
-
- Bröms, Jeanette E, 1974- (author)
- Umeå universitet,Klinisk bakteriologi,Molekylär Infektionsmedicin, Sverige (MIMS)
-
- Lavander, Moa (author)
- Umeå universitet,Klinisk bakteriologi,Molekylär Infektionsmedicin, Sverige (MIMS)
-
- Meyer, Lena, 1982- (author)
- Umeå universitet,Klinisk bakteriologi,Molekylär Infektionsmedicin, Sverige (MIMS)
- show more...
- show less...
- (creator_code:org_t)
- American Society for Microbiology, 2011
- 2011
- English.
- In: Infection and Immunity. - : American Society for Microbiology. - 0019-9567 .- 1098-5522. ; 79:9, s. 3683-3696
- Journal article (peer-reviewed)
Abstract
Subject headings
Close
- 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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Infektionsmedicin (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Infectious Medicine (hsv//eng)
Publication and Content Type
- ref (subject category)
- art (subject category)
Find in a library
- Infection and Immunity (Search for host publication in LIBRIS)
To the university's database
- 1 of 1
- Previous record
- Next record
- To hitlist
Find more in SwePub
- By the author/editor
- Bröms, Jeanette ...
- Lavander, Moa
- Meyer, Lena, 198 ...
- Sjöstedt, Anders ...
- About the subject
-
- MEDICAL AND HEALTH SCIENCES
- MEDICAL AND HEAL ...
- and Basic Medicine
- and Immunology in th ...
-
- MEDICAL AND HEALTH SCIENCES
- MEDICAL AND HEAL ...
- and Clinical Medicin ...
- and Infectious Medic ...
- Articles in the publication
- Infection and Im ...
- By the university
- Umeå University
Search outside SwePub
- Extend your search to:
- Google Book Search
- Google Scholar
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.
- Copyright © LIBRIS - National Library Systems
- LIBRIS.kb.se
