Linked Life Data

10415058

Source:http://linkedlifedata.com/resource/pubmed/id/10415058

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-8-12
pubmed:abstractText
How eosinophils are preferentially recruited to inflammatory sites remains elusive, but increasing evidence suggests that chemokines that bind to the CCR3 participate in this process. In this study, we investigated the transcript levels and chemotactic activity of CCR3-binding chemokines in nasal polyps, a disorder often showing prominent eosinophilia. We found that mRNA expression for eotaxin, eotaxin-2, and monocyte-chemotactic protein-4 was significantly increased in nasal polyps compared with turbinate mucosa from the same patients, or histologically normal nasal mucosa from control subjects. Interestingly, the novel CCR3-specific chemokine, eotaxin-2, showed the highest transcript levels. Consistent with these mRNA data, polyp tissue fluid exhibited strong chemotactic activity for eosinophils that was significantly inhibited by a blocking Ab against CCR3. When patients were treated systemically with glucocorticosteroids, the mRNA levels in the polyps were reduced to that found in turbinate mucosa for all chemokines. Together, these findings suggested an important role for CCR3-binding chemokines in eosinophil recruitment to nasal polyps. Such chemokines, therefore, most likely contribute significantly in the pathogenesis of eosinophil-related disorders; and the reduced chemokine expression observed after steroid treatment might reflect, at least in part, how steroids inhibit tissue accumulation of eosinophils.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1545-51
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10415058-Adult, pubmed-meshheading:10415058-Aged, pubmed-meshheading:10415058-Body Fluids, pubmed-meshheading:10415058-Chemokine CCL11, pubmed-meshheading:10415058-Chemokine CCL24, pubmed-meshheading:10415058-Chemokines, CC, pubmed-meshheading:10415058-Chemotactic Factors, Eosinophil, pubmed-meshheading:10415058-Chemotaxis, Leukocyte, pubmed-meshheading:10415058-Cytokines, pubmed-meshheading:10415058-Eosinophilia, pubmed-meshheading:10415058-Eosinophils, pubmed-meshheading:10415058-Female, pubmed-meshheading:10415058-Humans, pubmed-meshheading:10415058-Leukocyte Count, pubmed-meshheading:10415058-Male, pubmed-meshheading:10415058-Middle Aged, pubmed-meshheading:10415058-Monocyte Chemoattractant Proteins, pubmed-meshheading:10415058-Nasal Polyps, pubmed-meshheading:10415058-Prednisone, pubmed-meshheading:10415058-RNA, Messenger, pubmed-meshheading:10415058-Turbinates
pubmed:year
1999
pubmed:articleTitle
Glucocorticosteroids inhibit mRNA expression for eotaxin, eotaxin-2, and monocyte-chemotactic protein-4 in human airway inflammation with eosinophilia.
pubmed:affiliation
Laboratory for Immunohistochemistry, Institute of Pathology, Department of Ear, Nose, and Throat, University of Oslo, The National Hospital, Rikshospitalet, Norway. f.l.jahnsen@labmed.uio.no
pubmed:publicationType
Journal Article, Clinical Trial, Randomized Controlled Trial, Research Support, Non-U.S. Gov't