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Interleukin-5 is important for the development of eosinophilic rhinitis following toluene diisocyanate inhalation in mice.

Authors
Johnson-VJ; Kashon-ML; Reynolds-JS; Fluharty-K; Wang-W; Li-S; Yucesoy-B
Source
Eur Respir J 2009 Sep; 34(3)(Suppl 53):893s
NIOSHTIC No.
20036001
Abstract
Diisocyanate exposure is a leading causes of work-related respiratory allergies including occupational rhinitis and asthma. We have shown that inhalation of toluene diisocyanate (TDI) caused allergic rhinitis in mice with marked upregulation of interleukin (IL)-5 in the nasal mucosa. The present study utilized antibody-mediated neutralization of IL-5 to test the hypothesis that IL-5 plays a key role in allergic and/or eosinophilic inflammation in TDI-induced rhinitis. Mice were exposed to 50 ppb TDI vapor for 4 h/day for 12 weekdays. Gene expression was determined using Illumina whole-genome microarrays and Taqman PCR. Gene Ontology and network analysis confirmed that IL-5 was a key cytokine in many of the upregulated immune networks. In addition, TDI inhalation upregulated Th2 cytokine (IL-4, -5, -13, -10) and chemokine (Ccl11, Ccl24) expression and eosinophil infiltration into the nasal mucosa of mice with TDI rhinitis. The expression of the eosinophil genes eosinophil peroxidase (Epx) and siglec F were upregulated (7.7 fold, P=0.001 and 27.5 fold, P=0.001, respectively) in the nasal mucosa of mice with TDI rhinitis supporting the presence of eosinophilic inflammation. Neutralization of IL-5 did not affect the development of the cytokine/chemokine response driving recruitment of eosinophils. However, treatment with anti-IL-5 reduced infiltration of eosinophils and attenuated the expression of Epx (1.7 fold, P=0.667) and siglec F (4.4 fold, P=0.606) in the nasal mucosa. These results support a role for IL-5 in the regulation of eosinophilic airway inflammation in TDI-induced rhinitis. Supported in part by an NIEHS-NIOSH Interagency Agreement (Y1-ES-0001).
Keywords
Allergies; Biological-effects; Biological-factors; Cell-biology; Cell-damage; Cellular-reactions; Cytology; Exposure-methods; Genes; Genetic-factors; Humans; Inhalation-studies; Laboratory-animals; Microscopic-analysis; Microscopy; Nasal-disorders; Particle-aerodynamics; Particulates; Respiratory-hypersensitivity; Respiratory-irritants; Respiratory-system-disorders; Risk-factors; Statistical-analysis
Contact
Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Mailstop L-3014, Morgantown, WV 26505
CODEN
ERJOEI
Publication Date
20090801
Document Type
Abstract
Fiscal Year
2009
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
0903-1936
NIOSH Division
HELD
Priority Area
Services
Source Name
European Respiratory Journal. Abstracts 19th ERS Annual Congress, Vienna, Austria, September 12-16, 2009
State
WV
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