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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 1
pubmed:dateCreated
1999-5-17
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1073-449X
pubmed:author
pubmed:issnType
Print
pubmed:volume
159
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1074-80
pubmed:dateRevised
2006-11-15
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
pubmed:year
1999
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.
pubmed:affiliation
Department of Pharmacology and Pathophysiology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't