 The loss of deep inhalation bronchoprotection in asthmatic individuals has been shown to be related to the degree of airway hyperresponsiveness, a hallmark of asthma. In several studies, asthmatic individuals with mild airway hyperresponsiveness AHR methacholine PC20 2 mgmL had a difference in methacholine PC20 with and without deep inhalations that averaged 1.8 doubling methacholine concentrations p0.0003. Conversely, asthmatic individuals with moderate to severe AHR methacholine PC20 2 mgmL had a non-significant difference in methacholine PC20 with and without deep inhalations p0.09. This loss of deep inhalation bronchoprotection is also now believed to play an important role in the pathogenesis of asthma. Airway inflammation is another of the key features of asthma and information on airway inflammation is increasingly being used in the diagnosis and treatment of asthma. The level of airway inflammation as measured by fraction of exhaled nitric oxide and sputum eosinophilia has also been shown to be correlated to the level of airway hyperresponsiveness as measured by methacholine PC20. In addition, glucocorticoids have been shown to decrease airway hyperresponsiveness, further suggesting that these two phenomena, airway inflammation and airway hyperresponsiveness, are related. We therefore suggest that the degree of airway inflammation is related to the loss of deep inhalation bronchoprotection and expect there to be a negative correlation between the degree of deep inhalation bronchoprotection and airway inflammation. 