Interleukin-5 Is Important for the Development of Eosinophilic Rhinitis Following Toluene Diisocyanate Inhalation in Mice

Details

• Personal Author:
  Fluharty K ; Johnson VJ ; Kashon ML ; Li S ; Reynolds JS ; Wang W ; Yucesoy, Berran
• Description:
  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). [Description provided by NIOSH]
• Subjects:
  Biological Factors Cytology Genetics Hypersensitivity Irritants Laboratories Microbiology Nose Occupational Health Particulate Matter Respiratory Hypersensitivity Respiratory System Respiratory Tract Diseases Risk Assessment Risk Factors Safety Sense Organs

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• Keywords:
  Allergies Biological-effects Biological-factors Cell-biology Cell-damage Cellular-reactions 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

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• ISSN:
  0903-1936
• Document Type:
  Text
• Genre:
  Abstract or Summary
• Place as Subject:
  OSHA Region 3 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  34
• Issue:
  3
• NIOSHTIC Number:
  nn:20036001
• Citation:
  Eur Respir J 2009 Sep; 34(3)(Suppl 53):893s
• Contact Point Address:
  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
• Federal Fiscal Year:
  2009
• NORA Priority Area:
  Services
• Peer Reviewed:
  False
• Source Full Name:
  European Respiratory Journal. Abstracts 19th ERS Annual Congress, Vienna, Austria, September 12-16, 2009
• Supplement:
  53
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:de9e161096be3ac98b46254851d27a2a0a6156d54a9b0b2177e8264bc8a139c7ba344f5fc331290d2d1c806d2a737ae93faeeee7921d177e5f16f73c2e928880
• Download URL:
  https://stacks.cdc.gov/view/cdc/187631/cdc_187631_DS1.pdf
• File Type:
  [PDF - 132.03 KB ]