Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 1
pubmed:dateCreated
1997-4-24
pubmed:abstractText
The functional role of interleukin (IL)-4 in the development of airway hyperresponsiveness (AHR) and pulmonary eosinophilia in response to sensitization and challenge of mice with sheep red blood cells (SRBC) was examined. Control- and SRBC-sensitized A/J mice were treated with an antibody to the murine IL-4 receptor (anti-IL-4R) 3 days before intratracheal challenge with the antigen or vehicle only. Blockade of IL-4R significantly reduced antigen-induced AHR and prevented increases in goblet cells and bronchoalveolar lavage (BAL) eosinophils. Treatment with anti-IL-4R did not affect antigen-induced increases in lung mRNA and BAL protein levels of IL-5 and interferon-gamma or IL-4 mRNA but did significantly increase IL-4 protein levels. Antigen-induced AHR was not reduced by treatment with antibodies to the adhesion molecules, vascular cell adhesion molecule-1 and very late activation antigen-4. Administration of IL-4 over a 7-day period did not increase airway reactivity or induce any changes in BAL cell numbers in naive mice. These results demonstrate that IL-4 is necessary for in vivo development of antigen-induced AHR, goblet cell metaplasia, and pulmonary eosinophilia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Allergic Agents, http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal, http://linkedlifedata.com/resource/pubmed/chemical/Antigen-Antibody Complex, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD, http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/Integrin alpha4beta1, http://linkedlifedata.com/resource/pubmed/chemical/Integrins, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-4, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Lymphocyte Homing, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
272
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
L253-61
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9124376-Animals, pubmed-meshheading:9124376-Anti-Allergic Agents, pubmed-meshheading:9124376-Antibodies, Monoclonal, pubmed-meshheading:9124376-Antigen-Antibody Complex, pubmed-meshheading:9124376-Antigens, pubmed-meshheading:9124376-Antigens, CD, pubmed-meshheading:9124376-Bronchoalveolar Lavage Fluid, pubmed-meshheading:9124376-Cytokines, pubmed-meshheading:9124376-Integrin alpha4beta1, pubmed-meshheading:9124376-Integrins, pubmed-meshheading:9124376-Interleukin-4, pubmed-meshheading:9124376-Lung, pubmed-meshheading:9124376-Male, pubmed-meshheading:9124376-Mice, pubmed-meshheading:9124376-Mice, Inbred Strains, pubmed-meshheading:9124376-RNA, Messenger, pubmed-meshheading:9124376-Receptors, Interleukin, pubmed-meshheading:9124376-Receptors, Interleukin-4, pubmed-meshheading:9124376-Receptors, Lymphocyte Homing, pubmed-meshheading:9124376-Recombinant Proteins, pubmed-meshheading:9124376-Respiratory Hypersensitivity, pubmed-meshheading:9124376-Vascular Cell Adhesion Molecule-1
pubmed:year
1997
pubmed:articleTitle
Interleukin-4 receptor blockade prevents airway responses induced by antigen challenge in mice.
pubmed:affiliation
Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't