Linked Life Data

20434232

Source:http://linkedlifedata.com/resource/pubmed/id/20434232

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2010-5-24
pubmed:abstractText
In Pseudomonas aeruginosa, cell-cell communication based on acyl-homoserine lactone (HSL) quorum sensing molecules is known to coordinate the production of virulence factors and biofilms by the bacterium. Incidentally, these bacterial signals can also modulate mammalian cell behaviour. We demonstrate here that 3O-C(12)-HSL can induce changes in calcium signalling through influx and release of calcium from thapsigargin-sensitive stores and delocalization of inositol 1,4,5-trisphosphate receptors (IP(3)R), but not of ryanodine receptors (RyR). In parallel, P. aeruginosa 3O-C(12)-HSL disrupts junctions in human Caco-2 cells as evidenced by a reduction of the expression and distribution of ZO-3 and JAM-A. Using co-immunoprecipitation we also found an alteration in the binding of ZO-3 to JAM-A in protein complexes. Moreover, 3O-C(12)-HSL-treatment resulted in tyrosine hyperphosphorylation of ZO-3 and JAM-A. On the contrary, serine and threonine residues of ZO-1 and JAM-A became less phosphorylated after exposition of 3O-C(12)-HSL. The 3O-C(12)-HSL-induced intracellular calcium signalling and alteration in the phosphorylation status of junction proteins furthermore correlated with changes in the association between JAM-A-ZO-3. The calcium inhibitors thapsigargin, xestospongin C, and dantrolene partly prevented the 3O-C(12)-HSL-induced decreases in TER and increases in the paracellular flux of 10kDa dextran. These findings clearly suggest that P. aeruginosa 3O-C(12)-HSL can cause the loss of epithelial barrier function via calcium signalling and further alteration in the phosphorylation status of junction proteins; and that bacterial quorum sensing signals represent inter-kingdom signalling.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1618-1298
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Elsevier GmbH. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
584-97
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Role of calcium signalling and phosphorylations in disruption of the epithelial junctions by Pseudomonas aeruginosa quorum sensing molecule.
pubmed:affiliation
Division of Medical Microbiology, Department of Clinical and Experimental Medicine, Linköping University, SE-58185 Linköping, Sweden. elena.vikstrom@liu.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't