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

Authors


Correspondence:
Shiho Furusho, Department of Respiratory Medicine, Cellular Transplantation Biology, Kanazawa University Graduate School of Medical Science, 13-1 Takara-machi, Kanazawa-shi, Ishikawa 920-8641, Japan.
E-mail: sfurusho@med3.m.kanazawa-u.ac.jp

Summary

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-α, macrophage inflammatory protein-2 (MIP-2), IL-4, IL-5 and IFN-γ 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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