Literature DB >> 17257216

Airway inflammation and bronchial remodelling in toluene diisocyanate-exposed BALB/c mouse model.

L-Z Sun1, S Elsayed, A M Bronstad, T Van Do, A Irgens, N P Aardal, T B Aasen.   

Abstract

UNLABELLED: Toluene 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 microg OVA or pep absorbed on 300 microg alum, 300 microg alum or saline on days 0, 7 and 14. For the TDI group, mice were sensitized subcutaneously with 20 microl neat TDI on day 0; 20 microl of TDI in olive oil (1:10) on days 7 and 14; on days 21-23. Then each group was challenged intranasally with 20 microl 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-gamma 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.

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Year:  2007        PMID: 17257216     DOI: 10.1111/j.1365-3083.2006.01882.x

Source DB:  PubMed          Journal:  Scand J Immunol        ISSN: 0300-9475            Impact factor:   3.487


  3 in total

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Journal:  Int J Occup Environ Health       Date:  2014 Jan-Mar

2.  Histamine release and inflammatory cell infiltration in airway Mucosa in methylene diphenyl diisocyanate (MDI)-induced occupational asthma.

Authors:  Gyu-Young Hur; Seung-Soo Sheen; Young-Mi Kang; Dong-Hee Koh; Han-Jung Park; Young-Min Ye; Hyun-Ee Yim; Kyoo-Sang Kim; Hae-Sim Park
Journal:  J Clin Immunol       Date:  2008-05-17       Impact factor: 8.317

3.  Air pollutants and early origins of respiratory diseases.

Authors:  Dasom Kim; Zi Chen; Lin-Fu Zhou; Shou-Xiong Huang
Journal:  Chronic Dis Transl Med       Date:  2018-06-07
  3 in total

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