Linked Life Data

11755408

Source:http://linkedlifedata.com/resource/pubmed/id/11755408

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14-15
pubmed:dateCreated
2001-12-28
pubmed:abstractText
Salmonella typhimurium invades host macrophages and can induce either an almost immediate cell death or establish an intracellular niche within the phagocytic vacuole. Rapid cell death depends on the Salmonella pathogenicity island SPI1 and the host protein caspase-1, a member of the pro-apoptotic caspase family of proteases. Caspase-1-dependent cell death leads to the activation of the potent pro-inflammatory cytokines interleukin (IL)-1beta and IL-18 to produce bioactive cytokines. Animal studies indicate that the activation of these cytokines is necessary for efficient colonization of the mouse gastrointestinal tract. Salmonella that reside in the phagocytic vacuole do not cause this early cell death and can trigger a macrophage death at a much later time point. This late-phase cell death is dependent on SPI2-encoded genes and ompR.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1286-4579
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1201-12
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:articleTitle
Salmonella-induced macrophage death: the role of caspase-1 in death and inflammation.
pubmed:affiliation
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. dmonack@leland.stanford.edu
pubmed:publicationType
Journal Article, Review