Source:http://linkedlifedata.com/resource/pubmed/id/10586083
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2000-1-6
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pubmed:abstractText |
The NF-kappa B/Rel family of transcription factors induces many genes involved in immune and inflammatory responses. Mice with germline deletions of individual NF-kappa B/Rel subunits have different phenotypes, suggesting that the NF-kappa B/Rel transcription factors have different functions. We tested whether c-Rel promotes allergic asthma using a murine model of allergen-induced pulmonary inflammation and airway hyperresponsiveness. Our investigation focused on c-Rel, which is expressed in lymphoid cells and is important for lymphocyte activation. In response to allergen sensitization and challenge, c-Rel-deficient mice did not develop increases in pulmonary inflammation, bronchoalveolar lavage fluid eosinophilia, or total serum IgE. c-Rel deficiency also prevented the induction of airway hyperresponsiveness. Allergen-treated wild-type mice had increased DNA binding to an NF-kappa B consensus site. Chemokine expression was altered in allergen-treated c-Rel-deficient mice. Monocyte chemoattractant protein-1, which is regulated by NF-kappa B, was decreased in allergen-treated c-Rel-deficient mice relative to wild-type controls. The increase in NF-kappa B/Rel transcription factors after allergen challenge in wild-type mice and the decrease in allergen reactivity found in c-Rel-deficient mice indicate that c-Rel promotes allergic inflammation. Alteration of pulmonary chemokine expression in c-Rel-deficient mice may inhibit allergen-induced pulmonary inflammation and airway hyperresponsiveness.
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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/Aerosols,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin E,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-rel,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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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 |
163
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6827-33
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10586083-Aerosols,
pubmed-meshheading:10586083-Animals,
pubmed-meshheading:10586083-Bronchial Hyperreactivity,
pubmed-meshheading:10586083-Immunoglobulin E,
pubmed-meshheading:10586083-Injections, Intraperitoneal,
pubmed-meshheading:10586083-Lung,
pubmed-meshheading:10586083-Male,
pubmed-meshheading:10586083-Mice,
pubmed-meshheading:10586083-Mice, Inbred BALB C,
pubmed-meshheading:10586083-Mice, Inbred C57BL,
pubmed-meshheading:10586083-Mice, Knockout,
pubmed-meshheading:10586083-NF-kappa B,
pubmed-meshheading:10586083-Ovalbumin,
pubmed-meshheading:10586083-Proto-Oncogene Proteins c-rel,
pubmed-meshheading:10586083-RNA, Messenger,
pubmed-meshheading:10586083-Respiratory Hypersensitivity
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pubmed:year |
1999
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pubmed:articleTitle |
NF-kappa B/Rel transcription factors: c-Rel promotes airway hyperresponsiveness and allergic pulmonary inflammation.
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pubmed:affiliation |
Pulmonary Division, Brigham and Women's Hospital, Boston, MA 02115, 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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