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- Publisher
- Springer Journals
- Copyright
- Copyright © 2006 by Nature Publishing Group
- Subject
- Biomedicine; Biomedicine, general; Immunology; Infectious Diseases
- ISSN
- 1529-2908
- eISSN
- 1529-2916
- DOI
- 10.1038/ni1344
- Publisher site
- See Article on Publisher Site
Abstract
Macrophages respond to Salmonella typhimurium infection via Ipaf, a NACHT–leucine-rich repeat family member that activates caspase-1 and secretion of interleukin 1β. However, the specific microbial salmonella-derived agonist responsible for activating Ipaf is unknown. We show here that cytosolic bacterial flagellin activated caspase-1 through Ipaf but was independent of Toll-like receptor 5, a known flagellin sensor. Stimulation of the Ipaf pathway in macrophages after infection required a functional salmonella pathogenicity island 1 type III secretion system but not the flagellar type III secretion system; furthermore, Ipaf activation could be recapitulated by the introduction of purified flagellin directly into the cytoplasm. These observations raise the possibility that the salmonella pathogenicity island 1 type III secretion system cannot completely exclude 'promiscuous' secretion of flagellin and that the host capitalizes on this 'error' by activating a potent host-defense pathway.
Journal
Nature Immunology – Springer Journals
Published: Apr 30, 2006