rdf:type |
|
lifeskim:mentions |
umls-concept:C0026809,
umls-concept:C0123771,
umls-concept:C0205263,
umls-concept:C0332206,
umls-concept:C0458827,
umls-concept:C0597750,
umls-concept:C0871261,
umls-concept:C1292733,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
|
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
|