Source:http://linkedlifedata.com/resource/pubmed/id/18063698
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2008-2-27
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pubmed:abstractText |
Modulation of leukocyte recruitment through intervention with chemokine receptors is an attractive, therapeutic strategy. Recently, we have shown that n-Nonanoyl (NNY)-CCL14 internalizes and desensitizes human (h)CCR3, resulting in the inactivation of eosinophils. In this study, we investigated the interaction of NNY-CCL14 with CCR1 and CCR5 and the relevance of these NNY-CCL14 receptors on its in vivo effects in allergic airway inflammation. NNY-CCL14 has inactivating properties on CCR1(+) and CCR5(+) cell lines and primary leukocytes. It desensitizes hCCR1- and hCCR5-mediated calcium release and internalizes these receptors from the cellular surface. Treatment of OVA-sensitized BALB/c mice with NNY-CCL14 resulted in reduced pulmonary inflammation. Above all, it is demonstrated that systemic treatment with NNY-CCL14 down-modulates CCR5 from the surface of lymphocytes in vivo. Although NNY-CCL14 acts on murine lymphocytes and internalizes CCR5, it does not internalize CCR3 on mouse eosinophils, showing species selectivity regarding this particular receptor. Therefore, the inhibitory effects of NNY-CCL14 in murine models of allergic airway inflammation can be assigned to its interaction with CCR5. The presented results substantiate the relevance of CCR5 as a target for allergic airway inflammation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCR1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL11,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL3,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CC,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR5
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0741-5400
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pubmed:author |
pubmed-author:BraunArminA,
pubmed-author:ElsnerJörnJ,
pubmed-author:EscherSylvia ESE,
pubmed-author:ForssmannUlfU,
pubmed-author:ForssmannWolf-GeorgWG,
pubmed-author:FuchsBarbaraB,
pubmed-author:GuptaShipraS,
pubmed-author:HeitlandAleksandraA,
pubmed-author:MackMatthiasM,
pubmed-author:Schulz-MarondeSandraS,
pubmed-author:TillmannHanns-ChristianHC
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pubmed:issnType |
Print
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pubmed:volume |
83
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
765-73
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pubmed:meshHeading |
pubmed-meshheading:18063698-Animals,
pubmed-meshheading:18063698-Chemokine CCL11,
pubmed-meshheading:18063698-Chemokine CCL3,
pubmed-meshheading:18063698-Chemokines, CC,
pubmed-meshheading:18063698-Humans,
pubmed-meshheading:18063698-Hypersensitivity,
pubmed-meshheading:18063698-Inflammation,
pubmed-meshheading:18063698-Mice,
pubmed-meshheading:18063698-Ovalbumin,
pubmed-meshheading:18063698-Receptors, CCR1,
pubmed-meshheading:18063698-Receptors, CCR5,
pubmed-meshheading:18063698-T-Lymphocytes
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pubmed:year |
2008
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pubmed:articleTitle |
Intravascular inactivation of CCR5 by n-Nonanoyl-CC chemokine ligand 14 and inhibition of allergic airway inflammation.
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pubmed:affiliation |
Center of Pharmacology and Toxicology, Hannover Medical School, Feodor-Lynen-Strasse 31, 30625 Hannover, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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