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

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.