Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-12-16
pubmed:abstractText
During inflammation, host- and microbial-derived proteases trigger the activation of protease-activated receptors (PARs), a family of G-protein-coupled receptors. We report here that activation of Toll-like receptors (TLRs) by fungi unmasks an essential and divergent role for PAR(1) and PAR(2) in downstream signaling and inflammation. TLRs activated PARs and triggered distinct signal transduction pathways involved in inflammation and immunity to Candida albicans and Aspergillus fumigatus. Inflammation was promoted by PAR(1) and PAR(2) activation in response to Candida and by PAR(2) inhibition in response to Aspergillus. This occurred by TLR regulation of PAR signaling, with TLR2 promoting PAR(1) activity, and TLR4 suppressing PAR(2) activity. Thus, tissue injury and pathogens induce signals that are integrated at the level of distinct TLR/PAR-dependent pathways, the exploitation or subversion of which contributes to divergence in microbial promotion of inflammatory response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1935-3456
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
156-68
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
The contribution of PARs to inflammation and immunity to fungi.
pubmed:affiliation
Department of Experimental Medicine and Biochemical Science, University of Perugia, Via del Giochetto, Perugia, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't