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Prevention of IL-1 Signaling Attenuates Airway Hyperresponsiveness and Inflammation in a Murine Model of Toluene Diisocyanate-Induced Asthma

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  • Personal Author:
  • Description:
    IL-1 is a pleotropic cytokine that has been shown to play a prominent role in asthma induced by large-molecular-weight proteins. Increased IL-1 immunostaining in the submucosa of patients with toluene diisocyanate (TDI)-induced asthma has also been observed, suggesting that this cytokine might also be important in asthma associated with low-molecular-weight chemicals. We sought to determine the role of IL-1 signaling in airway reactivity and inflammation by using a murine model of TDI-induced asthma. C57BL/6 mice were exposed to TDI by means of vapor inhalation (20 ppb; 4 hours per day, 5 days per week, for 6 weeks) and then challenged 2 weeks later by inhalation with 20 ppb TDI vapor for 1 hour. Sensitized-challenged mice showed increased airway hyperresponsiveness (AHR), increased levels of TDI-specific IgG1 antibodies, airway epithelial thickening, inflammation consisting of infiltrating lymphocytes and eosinophils, and increased mRNA expression of IL-4, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 in the lung. Prevention of IL-1 signaling through deletion of the IL-1 receptor type I or administration of neutralizing antibodies to both IL-1beta and IL-1alpha abrogated the development of TDI-induced asthma. A partial reduction in AHR and TDI-specific IgG1 levels was observed in mice administered anti-IL-1beta, whereas anti-IL-1alpha had no effect on either parameter. Antibodies to IL-1beta or IL-1alpha alone blocked airway inflammation and the expression of IL-4 and adhesion molecules in the lung. These results suggest that IL-1 signaling is critical for AHR and airway inflammation, with IL-1beta and IL-1alpha having unique and overlapping roles in TDI-induced occupational asthma. [Description provided by NIOSH]
  • Subjects:
  • Keywords:
  • ISSN:
    0091-6749
  • Document Type:
    Text
  • Genre:
    Journal Article
  • Place as Subject:
  • CIO:
    National Institute for Occupational Safety and Health (NIOSH)
  • Division:
    HELD - Health Effects Laboratory Division
  • Topic:
    Workplace Safety & Health
  • Location:
    North America
  • Volume:
    116
  • Issue:
    4
  • NIOSHTIC Number:
    nn:20028553
  • Citation:
    J Allergy Clin Immunol 2005 Oct; 116(4):851-858
  • Contact Point Address:
    Victor J. Johnson, PhD, Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Rd, Mail Stop 3014, Morgantown, WV 26505-2888
  • Email:
    vjohnson3@cdc.gov
  • Federal Fiscal Year:
    2006
  • NORA Priority Area:
    Disease and Injury: Asthma and Chronic Obstructive Pulmonary Disease
  • Peer Reviewed:
    True
  • Source Full Name:
    Journal of Allergy and Clinical Immunology
  • Collection(s):
  • Main Document Checksum:
    urn:sha-512:be9465066e4824741de0a44ab5558696b537f3bf341965283508ead2bdfc37fe3162c5fe2f7e5a379deae88b7ed168e8b727d85fbca870f4f46e6122c78919c9
  • Download URL:
  • File Type:
    Filetype[PDF - 281.66 KB ]
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