Linked Life Data

11780065

Source:http://linkedlifedata.com/resource/pubmed/id/11780065

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6866
pubmed:dateCreated
2002-1-7
pubmed:abstractText
Inappropriate or prolonged inflammation is the main cause of many diseases; for this reason it is important to understand the physiological mechanisms that terminate inflammation in vivo. Agonists for several Gs-protein-coupled receptors, including cell-surface adenosine purinergic receptors, can increase levels of immunosuppressive cyclic AMP in immune cells; however, it was unknown whether any of these receptors regulates inflammation in vivo. Here we show that A2a adenosine receptors have a non-redundant role in the attenuation of inflammation and tissue damage in vivo. Sub-threshold doses of an inflammatory stimulus that caused minimal tissue damage in wild-type mice were sufficient to induce extensive tissue damage, more prolonged and higher levels of pro-inflammatory cytokines, and death of male animals deficient in the A2a adenosine receptor. Similar observations were made in studies of three different models of inflammation and liver damage as well as during bacterial endotoxin-induced septic shock. We suggest that A2a adenosine receptors are a critical part of the physiological negative feedback mechanism for limitation and termination of both tissue-specific and systemic inflammatory responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:volume
414
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
916-20
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:articleTitle
Role of G-protein-coupled adenosine receptors in downregulation of inflammation and protection from tissue damage.
pubmed:affiliation
Laboratory of Immunology, National Institute of Allegy and Infectious Diseases, National Institutes of Health, 10 Center Drive, Bethesa, MD 20892-1892, USA.
pubmed:publicationType
Journal Article