Source:http://linkedlifedata.com/resource/pubmed/id/10194148
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4 Pt 1
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pubmed:dateCreated |
1999-5-17
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pubmed:abstractText |
Toluene diisocyanate (TDI) is a low-molecular-weight compound which is known to cause occupational asthma in 5 to 10% of exposed workers. Previously, we developed a murine model to investigate TDI-induced occupational asthma. Short-term exposure to TDI (skin sensitization twice daily on Day 0 and Day 1 and intranasal challenge on Day 8) led to a nonspecific tracheal hyperractivity 24 h after the challenge in TDI-sensitized mice when compared with nonsensitized mice whereas no TDI-specific IgE antibodies were found in the serum. Because 20% of subjects with TDI-induced occupational asthma exhibit an increase in serum IgE antibodies, we exposed mice for a longer period of time to investigate whether this procedure could induce TDI-specific antibody production in exposed mice. Long-term exposure (skin sensitization on 6 consecutive weeks followed by intranasal challenge on Week 7) resulted in the production of total IgE and IgG and TDI-specific IgE and IgG antibodies. Airway reactivity to various agonists was also measured in vitro and in vivo in long-term exposed mice. TDI-sensitized mice exhibited in vitro tracheal hyperreactivity to carbachol 3 h after the challenge when compared with the nonsensitized mice. Moreover, in vivo airway hyperresponsiveness to serotonin (5-hydroxytryptamine [5HT]) was found 3 h after the challenge in TDI-sensitized mice. Interestingly, in vivo airway hyperresponsiveness was not observed at any time point in the mice exposed to TDI according to the short-term protocol. In conclusion, by altering the exposure time and/or cumulative dosage of TDI different biological reactions can be elicited in exposed mice. This important finding might be a reflection of the diversity of symptoms found in patients suffering from TDI-induced asthma. Both the short-exposure and the long-exposure model will be useful to further investigate the mechanisms of action of TDI.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1073-449X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
159
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1074-80
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10194148-Administration, Intranasal,
pubmed-meshheading:10194148-Administration, Topical,
pubmed-meshheading:10194148-Airway Resistance,
pubmed-meshheading:10194148-Animals,
pubmed-meshheading:10194148-Antibody Formation,
pubmed-meshheading:10194148-Bronchial Hyperreactivity,
pubmed-meshheading:10194148-Immunization,
pubmed-meshheading:10194148-Immunoglobulin E,
pubmed-meshheading:10194148-Immunoglobulin G,
pubmed-meshheading:10194148-Lung,
pubmed-meshheading:10194148-Male,
pubmed-meshheading:10194148-Mice,
pubmed-meshheading:10194148-Mice, Inbred BALB C,
pubmed-meshheading:10194148-Respiratory Hypersensitivity,
pubmed-meshheading:10194148-Skin Tests,
pubmed-meshheading:10194148-Time Factors,
pubmed-meshheading:10194148-Toluene 2,4-Diisocyanate,
pubmed-meshheading:10194148-Trachea
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pubmed:year |
1999
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pubmed:articleTitle |
Long-term topical exposure to toluene diisocyanate in mice leads to antibody production and in vivo airway hyperresponsiveness three hours after intranasal challenge.
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pubmed:affiliation |
Department of Pharmacology and Pathophysiology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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