Role of intercellular adhesion molecule-1 in a murine model of toluene diisocyanate-induced asthma.

نویسندگان

  • S Furusho
  • S Myou
  • M Fujimura
  • T Kita
  • M Yasui
  • K Kasahara
  • S Nakao
  • K Takehara
  • S Sato
چکیده

BACKGROUND Adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) are thought to contribute to the airway inflammation and airway hyper-responsiveness (AHR) of allergic asthma. Some differences from allergic asthma have been noted, including airway neutrophilia, and the involvement of ICAM-1 in toluene diisocyanate (TDI) asthma is currently unclear. OBJECTIVE We utilized mice lacking ICAM-1 expression (ICAM-1(-/-)) to investigate the role of ICAM-1 in airway inflammation and AHR in TDI-induced asthma. METHODS Male C57BL/6J mice (ICAM-1(+/+)) and ICAM-1(-/-) mice were intranasally sensitized to TDI solution or solvent alone. Airway inflammation, AHR and cytokine secretion were assessed 24 h after challenge by TDI or solvent. The production of antigen-specific IgG and IgE by TDI sensitized and non-sensitized mice was determined. RESULTS TDI challenge to ICAM-1(+/+) mice induced an increase in airway inflammatory cell numbers, AHR and cytokine secretion of TNF-alpha, macrophage inflammatory protein-2 (MIP-2), IL-4, IL-5 and IFN-gamma into the bronchoalveolar lavage fluid. All these pathophysiological changes were reduced in ICAM-1(-/-) mice. Serum levels of TDI-specific IgG and IgE of ICAM-1(-/-) and ICAM-1(+/+) mice were comparable. CONCLUSION These results suggest that ICAM-1 plays an essential role in airway inflammation and AHR in TDI-induced asthma.

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عنوان ژورنال:
  • Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology

دوره 36 10  شماره 

صفحات  -

تاریخ انتشار 2006