Source:http://linkedlifedata.com/resource/pubmed/id/11290802
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2001-4-6
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pubmed:abstractText |
To evaluate the role of CCR2 in allergic asthma, mutant mice deficient in CCR2 (CCR2(-/-)) and intact mice were sensitized with i.p. OVA with alum on days 0 and 7, and challenged by inhalation with nebulization of either OVA or saline. Airway hyperreactivity, measured by the methacholine-provoked increase in enhanced pause, was significantly increased (p < 0.05) in OVA-challenged CCR2(-/-) mutant mice, compared with comparably challenged CCR2(+/+) mice. OVA-challenged CCR2(-/-) mutants also were also found to have enhanced bronchoalveolar lavage fluid eosinophilia, peribronchiolar cellular cuffing, and Ig subclass switching, with increase in OVA-specific IgG(1) and IgE. In addition, RNase protection assay revealed increased whole lung expression of IL-13 in OVA-challenged CCR2(-/-) mutants. Unexpectedly, serum monocyte chemotactic protein-1 levels were 8-fold higher in CCR2(-/-) mutants than in CCR2(+/+) mice sensitized to OVA, but OVA challenge had no additional effect on circulating monocyte chemotactic protein-1 in either genotype. Ag stimulation of lymphocytes isolated from OVA-sensitized CCR2 mutants revealed a significant increase (p < 0.05) in IL-5 production, which differed from OVA-stimulated lymphocytes from sensitized CCR2(+/+) mice. These experiments demonstrate an enhanced response in airway reactivity and in lung inflammation in CCR2(-/-) mutant mice compared with comparably sensitized and challenged CCR2(+/+) mice. These observations suggest that CC chemokines and their receptors are involved in immunomodulation of atopic asthma.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Allergens,
http://linkedlifedata.com/resource/pubmed/chemical/Bronchoconstrictor Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Ccr2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin E,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Methacholine Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
166
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
5183-92
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11290802-Administration, Inhalation,
pubmed-meshheading:11290802-Allergens,
pubmed-meshheading:11290802-Animals,
pubmed-meshheading:11290802-Asthma,
pubmed-meshheading:11290802-Bronchial Hyperreactivity,
pubmed-meshheading:11290802-Bronchoalveolar Lavage Fluid,
pubmed-meshheading:11290802-Bronchoconstrictor Agents,
pubmed-meshheading:11290802-Chemokine CCL2,
pubmed-meshheading:11290802-Disease Models, Animal,
pubmed-meshheading:11290802-Eosinophilia,
pubmed-meshheading:11290802-Immunoglobulin E,
pubmed-meshheading:11290802-Immunoglobulin G,
pubmed-meshheading:11290802-Injections, Intraperitoneal,
pubmed-meshheading:11290802-Lung,
pubmed-meshheading:11290802-Lymphocyte Activation,
pubmed-meshheading:11290802-Methacholine Chloride,
pubmed-meshheading:11290802-Mice,
pubmed-meshheading:11290802-Mice, Inbred C57BL,
pubmed-meshheading:11290802-Mice, Inbred Strains,
pubmed-meshheading:11290802-Mice, Knockout,
pubmed-meshheading:11290802-Ovalbumin,
pubmed-meshheading:11290802-Receptors, CCR2,
pubmed-meshheading:11290802-Receptors, Chemokine,
pubmed-meshheading:11290802-Th2 Cells
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pubmed:year |
2001
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pubmed:articleTitle |
Enhanced airway Th2 response after allergen challenge in mice deficient in CC chemokine receptor-2 (CCR2).
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pubmed:affiliation |
Division of Pulmonary and Critical Care Medicine, and Division of Rheumatology and Immunology, University of Virginia Health System, Charlottesville, VA 22908, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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