Linked Life Data

16759878

Source:http://linkedlifedata.com/resource/pubmed/id/16759878

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
2006-7-18
pubmed:abstractText
Excessive production of proinflammatory cytokines, including TNF-alpha, IL-1, IL-6, IL-12, and IFN-gamma is thought to contribute significantly to lethality in septic shock syndromes. IL-23 is a heterodimeric cytokine that combines the p40 subunit of IL-12 with a specific p19 subunit. Similar to IL-12, IL-23 is considered to be a key immunoregulator in the response to pathogenic organisms but its contribution to Gram-negative endotoxic shock is as yet unclear. Using an established shock model with Pseudomonas aeruginosa, we found early and sustained expression of IL-23 p19 transcripts in the spleens of mice undergoing lethal challenge with the bacterium. Administration of p19-neutralizing antibody reduced mortality in a dose-dependent fashion. Survival in P. aeruginosa-challenged mice was associated with a dramatic decrease in circulating levels of the pathogenetic cytokines, TNF-alpha and IFN-gamma. Hence, IL-23 may represent a new therapeutic target in Gram-negative endotoxic shock.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1043-4666
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
161-9
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
IL-23 neutralization protects mice from Gram-negative endotoxic shock.
pubmed:affiliation
Department of Experimental Medicine and Biochemical Sciences, Section of Pharmacology, University of Perugia, Via del Giochetto, Perugia 06126, Italy. laurabell@tin.it
pubmed:publicationType
Journal Article