|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0007589,
umls-concept:C0014457,
umls-concept:C0026727,
umls-concept:C0035820,
umls-concept:C0037083,
umls-concept:C0155877,
umls-concept:C0458827,
umls-concept:C1511545,
umls-concept:C1511938,
umls-concept:C1527148,
umls-concept:C1710082
|
|
pubmed:issue |
10
|
|
pubmed:dateCreated |
2004-9-20
|
|
pubmed:abstractText |
When wild-type BALB/c mice were transferred with OVA-specific Th2 cells followed by OVA inhalation, a severe eosinophilia, mucus hypersecretion and airway hyper-responsiveness (AHR) was induced in parallel with a marked elevation of IL-4, IL-5 and IL-13 levels in bronchoalveolar lavage fluid (BALF). However, neither eosinophilia, AHR nor mucus hypersecretion was induced in Th2 cell-transferred STAT6-/- mice. The failure of eosinophilia was not due to the defect of Th2 cytokine production in BALF of STAT6-/- mice transferred with Th2 cells, but because of the defect of STAT6-dependent eotaxin production. Indeed, intranasal administration of eotaxin reconstituted pulmonary eosinophilia but not AHR and mucus hypersecretion in OVA-inhalated STAT6-/- mice. These results initially provided direct evidence that STAT6-dependent eotaxin production is essential for pulmonary eosinophilia. We also dissociated the role of STAT6 for eosinophilia from that for AHR and mucus hypersecretion. Thus, STAT6 also plays a critical role at late phase of Th2-dependent allergy induction.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Ccl11 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL11,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CC,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/STAT6 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Stat6 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Oct
|
|
pubmed:issn |
0953-8178
|
|
pubmed:author |
pubmed-author:AsakuraYumikoY,
pubmed-author:AshinoShigeruS,
pubmed-author:ChamotoKenjiK,
pubmed-author:HoshinoAkihikoA,
pubmed-author:IkedaHiroakiH,
pubmed-author:JinushiTakafumiT,
pubmed-author:MatsuzakiJunkoJ,
pubmed-author:MitaYasuoY,
pubmed-author:NakaikeShiroS,
pubmed-author:NishimuraTakashiT,
pubmed-author:SakuraiTakanobuT,
pubmed-author:TakaokaAkikoA,
pubmed-author:TakeshimaTsuguhideT,
pubmed-author:TanakaYoshitakaY,
pubmed-author:TeramuraTakashiT,
pubmed-author:TsujiTakemasaT
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
16
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
1497-505
|
|
pubmed:dateRevised |
2007-11-15
|
|
pubmed:meshHeading |
pubmed-meshheading:15351784-Administration, Intranasal,
pubmed-meshheading:15351784-Animals,
pubmed-meshheading:15351784-Asthma,
pubmed-meshheading:15351784-Bronchial Hyperreactivity,
pubmed-meshheading:15351784-Bronchoalveolar Lavage Fluid,
pubmed-meshheading:15351784-Cell Differentiation,
pubmed-meshheading:15351784-Chemokine CCL11,
pubmed-meshheading:15351784-Chemokines, CC,
pubmed-meshheading:15351784-Eosinophilia,
pubmed-meshheading:15351784-Hypersensitivity,
pubmed-meshheading:15351784-Lung,
pubmed-meshheading:15351784-Mice,
pubmed-meshheading:15351784-Mucus,
pubmed-meshheading:15351784-Ovalbumin,
pubmed-meshheading:15351784-Recombinant Proteins,
pubmed-meshheading:15351784-STAT6 Transcription Factor,
pubmed-meshheading:15351784-Th2 Cells,
pubmed-meshheading:15351784-Trans-Activators
|
|
pubmed:year |
2004
|
|
pubmed:articleTitle |
STAT6-mediated signaling in Th2-dependent allergic asthma: critical role for the development of eosinophilia, airway hyper-responsiveness and mucus hypersecretion, distinct from its role in Th2 differentiation.
|
|
pubmed:affiliation |
Medicinal Research Laboratory, Taisho Pharmaceutical Co, Ltd, Saitama, Japan.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
