Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-7-15
pubmed:abstractText
Ischemic-reperfusion injury (IRI) can affect many organ systems. Examples include strokes, coronary occlusion, accidental hypothermia, compartment syndrome and neonatal hypoxia. To date no mechanism has been fully accepted to explain acute inflammation associated with IRI. There is circumstantial evidence from animal and human ex-vivo cardiac experiments to support the hypothesis that acute inflammation associated with IRI is in part caused by IL-1 beta and/or IL-1 alpha secretion. Danger signal formation, such as uric acid/calcium pyrophosphate crystallization and other cellular stresses, may occur in IRI. These in turn may stimulate innate immune pathways (i.e. cryopyrin-inflammasome; and/ or toll-like receptors 2 and 4) to secrete IL-1 beta. Most IL-1 targeted therapy studies have focused on chronic human diseases and hopefully this discussion will create a framework to encourage use of this therapy in acute inflammation associated with IRI.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1521-7035
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
127-32
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Ischemic-reperfusion syndromes: biochemical and immunologic rationale for IL-1 targeted therapy.
pubmed:affiliation
Pediatrics, University of Colorado Health Sciences Center, 2055 North 22nd Avenue, Bozeman, MT 59718, USA. aw@aacmt.com
pubmed:publicationType
Journal Article, Review