Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2001-4-6
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5183-92
pubmed:dateRevised
2007-11-15
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
pubmed:year
2001
pubmed:articleTitle
Enhanced airway Th2 response after allergen challenge in mice deficient in CC chemokine receptor-2 (CCR2).
pubmed:affiliation
Division of Pulmonary and Critical Care Medicine, and Division of Rheumatology and Immunology, University of Virginia Health System, Charlottesville, VA 22908, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't