Source:http://linkedlifedata.com/resource/pubmed/id/10502558
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1999-11-10
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pubmed:abstractText |
We previously defined a role for B cells and allergen-specific immunoglobulins in the development of allergic sensitization, airway inflammation, and airway hyperresponsiveness (AHR), using a 10-d protocol in which allergen exposure occurred exclusively via the airways, without adjuvant. In the present protocol, normal and B-cell-deficient (microMt(-/-)) mice were sensitized intraperitoneally to ovalbumin (OVA) and challenged with OVA via the airways in order to examine the requirements for AHR with this protocol. T-cell activation (antigen-specific proliferative responses and Th2-type cytokine production) and eosinophil infiltration in the peribronchial regions of the airways, with signs of eosinophil activation and degranulation, occurred in both experimental groups. In contrast to the 10-d protocol, increased in vivo airway responsiveness to methacholine and in vitro tracheal smooth-muscle responses to electrical field stimulation were observed in both normal and B-cell-deficient mice, and these responses were inhibited by anti-interleukin (IL)-5 administration before airway challenge. These data show that IL-5, but not B cells or allergen-specific IgE, are required for eosinophil airway infiltration and the development of AHR following allergen/alum sensitization and repeated airway challenge with allergen. These results emphasize that the use of different sensitization and challenge protocols can influence the requirements for development of AHR.
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pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Allergens,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin E,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-5,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1044-1549
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
480-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10502558-Allergens,
pubmed-meshheading:10502558-Animals,
pubmed-meshheading:10502558-Asthma,
pubmed-meshheading:10502558-B-Lymphocytes,
pubmed-meshheading:10502558-Bronchial Hyperreactivity,
pubmed-meshheading:10502558-Cytokines,
pubmed-meshheading:10502558-Disease Models, Animal,
pubmed-meshheading:10502558-Eosinophilia,
pubmed-meshheading:10502558-Female,
pubmed-meshheading:10502558-Humans,
pubmed-meshheading:10502558-Immunoglobulin E,
pubmed-meshheading:10502558-Interleukin-5,
pubmed-meshheading:10502558-Mice,
pubmed-meshheading:10502558-Mice, Inbred C57BL,
pubmed-meshheading:10502558-Mice, Knockout,
pubmed-meshheading:10502558-Ovalbumin,
pubmed-meshheading:10502558-T-Lymphocytes
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pubmed:year |
1999
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pubmed:articleTitle |
Development of eosinophilic airway inflammation and airway hyperresponsiveness requires interleukin-5 but not immunoglobulin E or B lymphocytes.
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pubmed:affiliation |
Division of Basic Sciences and Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80260, 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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