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dc.contributor.authorSun, Li-Zhieng
dc.contributor.authorElsayed, S.eng
dc.contributor.authorBronstad, A. M.eng
dc.contributor.authorVan Do, T.eng
dc.contributor.authorIrgens, Ågoteng
dc.contributor.authorAardal, N. P.eng
dc.contributor.authorAasen, T. B.eng
dc.date.accessioned2012-06-28T07:37:25Z
dc.date.available2012-06-28T07:37:25Z
dc.date.issued2007eng
dc.identifier.citationScandinavian Journal of Immunology 65(2): 118–125.en
dc.identifier.issn0300-9475eng
dc.identifier.urihttp://hdl.handle.net/1956/5864
dc.description.abstractToluene diisocyanate (TDI), a highly reactive industrial chemical, is one of the leading causes of occupation-related asthma in industrialized countries. The pathogenesis of TDI-induced asthma, however, remains not fully understood, in part due to lack of appropriate animal models. Twenty five female BALB/c mice (age: 8 weeks) were randomly divided into 5 groups: Ovabumin (OVA); OVA peptide amino acid residues No. 323–339 (Pep); TDI; alum and physiological saline. Mice were intraperitoneally injected with 25 lg OVA or pep absorbed on 300 lg alum, 300 lg alum or saline on days 0, 7 and 14. For the TDI group, mice were sensitized subcutaneously with 20 ll neat TDI on day 0; 20 ll of TDI in olive oil (1:10) on days 7 and 14; on days 21–23. Then each group was challenged intranasally with 20 ll of 1% OVA, 1% Pep, 1% TDI, 10% alum and saline respectively. On day 28, mice were killed under pentothal anesthesia. The results demonstrated that neutrophil-dominant inflammation with a few eosinophil infiltration occurred in the peri-bronchial and peri-vascular regions of the lungs. This was accompanied by hyperplasia/ hypertrophy of cells lining the airways and mucus production as shown by HE staining. Positive immunohistochemical MBP staining in parenchyma was also shown. Th2 cytokine IL-4 and IgE production were significant increased 5 days after last challenge while IFN-c level was below the detection limit. Conclusion: the clear elevation of IL-4 and IgE could allow to conclude a possible Th2-like dominated allergic response in TDI-exposed BALB/c mouse model.en
dc.language.isoengeng
dc.publisherBlackwell Publishing Ltd.eng
dc.relation.ispartof<a href="http://hdl.handle.net/1956/5866" target="blank">Toluene diisocyanate (TDI)-induced asthma: Inflammatory and immunological responses to TDI, ovalbumin (OVA) and ovalbumin peptide OVA 323-339 in mouse models</a>eng
dc.titleAirway Inflammation and Bronchial Remodelling in Toluene Diisocyanate-exposed BALB/c Mouse Modeleng
dc.typePeer reviewedeng
dc.typeJournal articleeng
dc.subject.nsiVDP::Medical disciplines: 700::Basic medical, dental and veterinary science disciplines: 710::Medical immunology: 716eng
dc.rights.holderCopyright 2006 The Authors. Journal compilation Copyright 2006 Blackwell Publishing Ltd. Scandinavian Journal of Immunology.
dc.type.versionacceptedVersioneng
bora.peerreviewedPeer reviewedeng
bora.cristinID393891eng
bibo.doihttp://dx.doi.org/10.1111/j.1365-3083.2eng
dc.identifier.cristinID393891eng
dc.identifier.doihttp://dx.doi.org/10.1111/j.1365-3083.2
dcterms.isPartOfhttp://hdl.handle.net/1956/5866


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