ORIGINAL PAPER
Immunological determinants in a murine model of toluene diisocyanate-induced asthma
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1
Centre of Occupational Allergy and Environmental Health, Nofer Institute of Occupational Medicine, Łódź, Poland
2
Centre of Occupational Allergy and Environmental Health, Nofer Institute of Occupational Medicine, św. Teresy 8, 91-348, Łódź, Poland
3
Department of Occupational Diseases and Toxicology, Nofer Institute of Occupational Medicine, Łódź, Poland
4
Research Laboratory of Medicine and Veterinary Products in the GMP Quality, Nofer Institute of Occupational Medicine, Łódź, Poland
5
Department of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, Łódź, Poland
Int J Occup Med Environ Health. 2012;25(4):492-8
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ABSTRACT
Objectives: Diisocyanates (DIC) are highly reactive, low-molecular-weight chemicals which are the leading cause of occupational asthma (OA). The aim of the study was to analyze certain aspects of the pathogenesis of allergic infl ammation in the airways induced by toluene diisocyanate (TDI) in an experimental model in mice. Materials and Methods: The experiment was carried out on 50 female BALB/cJ/Han/IMP mice, which were exposed by inhalation (intranasal and in the inhalation chamber) to toluene diisocyanate (2,4-TDI). After the experiment, the bronchoalveolar lavage fluid (BALF) was collected from the animals, and the composition of the induced infl ammatory cells, and the concentrations of certain cytokines (IL-4, IL-5, TNF-α) were evaluated. Results: The total number of cells in BALF of the examined group of mice was signifi cantly higher compared to the control mice. There was also a signifi cant increase in neutrophils and eosinophils in the study group compared to the controls. The number of lymphocytes and macrophages did not differ signifi cantly between the two groups. A statistically signifi cant increase in the level of TNF-α was shown to occur in the group exposed to toluene diisocyanate in comparison to the control group. The concentration of IL-4 increased in the study group, compared to the control one, but the differences did not reach the level of signifi cance, p > 0.05. Such difference was not observed for IL-5. Conclusions: We developed a murine model of TDI-induced asthma which caused the infl ux of infl ammatory cells like eosinophils and neutrophils in the bronchoalveolar lavage fl uid (BALF) in the TDI-treated mice. The increase of the concentration of some proinfl ammatory cytokines (TNF-α, IL-4) in BALF from the exposed mice was also observed.