Linked Life Data

10438957

Source:http://linkedlifedata.com/resource/pubmed/id/10438957

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-9-9
pubmed:abstractText
Bronchial eosinophil and mononuclear cell infiltrates are a hallmark of the asthmatic lung and are associated with the induction of reversible airway hyperreactivity. In these studies, we have found that monocyte chemotactic protein-1 (MCP-1), a CC (beta) chemokine, mediates airway hyperreactivity in normal and allergic mice. Using a murine model of cockroach Ag-induced allergic airway inflammation, we have demonstrated that anti-MCP-1 Abs inhibit changes in airway resistance and attenuate histamine release into the bronchoalveolar lavage, suggesting a role for MCP-1 in mast cell degranulation. In normal mice, instillation of MCP-1 induced prolonged airway hyperreactivity and histamine release. In addition, MCP-1 directly induced pulmonary mast cell degranulation in vitro. These latter effects would appear to be selective because no changes were observed when macrophage-inflammatory protein-1alpha, eotaxin, or MCP-3 were instilled into the airways of normal mice or when mast cells were treated in vitro. Airway hyperreactivity was mediated by MCP-1 through CCR2 because allergen-induced as well as direct MCP-1 instilled-induced changes in airway hyperreactivity were significantly attenuated in CCR2 -/- mice. The neutralization of MCP-1 in allergic animals and instillation of MCP-1 in normal animals was related to leukotriene C4 levels in the bronchoalveolar lavage and was directly induced in pulmonary mast cells by MCP-1. Thus, these data identify MCP-1 and CCR2 as potentially important therapeutic targets for the treatment of hyperreactive airway disease.
pubmed:grant
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
15
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2160-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10438957-Administration, Intranasal, pubmed-meshheading:10438957-Airway Resistance, pubmed-meshheading:10438957-Allergens, pubmed-meshheading:10438957-Animals, pubmed-meshheading:10438957-Bronchial Hyperreactivity, pubmed-meshheading:10438957-Cells, Cultured, pubmed-meshheading:10438957-Chemokine CCL2, pubmed-meshheading:10438957-Cockroaches, pubmed-meshheading:10438957-Female, pubmed-meshheading:10438957-Histamine Release, pubmed-meshheading:10438957-Immunization, Secondary, pubmed-meshheading:10438957-Injections, Intraperitoneal, pubmed-meshheading:10438957-Intubation, Intratracheal, pubmed-meshheading:10438957-Leukotriene C4, pubmed-meshheading:10438957-Mast Cells, pubmed-meshheading:10438957-Mice, pubmed-meshheading:10438957-Mice, Inbred C57BL, pubmed-meshheading:10438957-Mice, Inbred CBA, pubmed-meshheading:10438957-Mice, Knockout, pubmed-meshheading:10438957-Receptors, CCR2, pubmed-meshheading:10438957-Receptors, Chemokine, pubmed-meshheading:10438957-Receptors, Cytokine
pubmed:year
1999
pubmed:articleTitle
Monocyte chemoattractant protein-1 mediates cockroach allergen-induced bronchial hyperreactivity in normal but not CCR2-/- mice: the role of mast cells.
pubmed:affiliation
Department of Pathology, Division of Pulmonary and Critical Care, University of Michigan Medical School, Ann Arbor 48109, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.