William J. Calhoun

The Role of Eosinophils in the Pathophysiology of Asthma

From current information, a number of conclusions can be drawn. Antigen activation of the allergic reaction in the airways is associated with an immediate rise in mast cell derived mediators, including histamine and tryptase. Associated with antigen activation of the allergic reaction is recruitment of eosinophils to the airways. This can best be seen in the airway lavage 48 hours after challenge with antigen. An increased presence of eosinophils suggests that they are an important contributor to the late allergic reaction and may be one of the major constituents in the development of bronchial inflammation. Although many factors participate in the late allergic inflammatory response, eosinophil-derived proteins are known to cause airway injury. Regulation of eosinophils in this process is not clearly established; however, our findings of increased IL-5 in relationship to the presence of eosinophils and their granular proteins suggests that this cytokine may be an important modulator of eosinophil function and activation following allergen challenge. However, much remains unknown in understanding bronchial inflammation and the eosinophils role in the process. In conclusion, the eosinophil is a major cellular participant in late phase allergic airway disease. Its presence and known functions suggest that the eosinophil is a significant cellular factor in the development of allergic airways disease in asthma. Further advances in this area will follow continued studies, particularly those which involve biopsy and correlation with airway physiology.

Hyperpigmentation, neutrophilic alveolitis, and erythema nodosum resulting from minocycline

Hyperpigmentation, pulmonary infiltration, and erythema nodosum occurred in a patient receiving long-term minocycline therapy. Bronchoalveolar lavage revealed both a neutrophilic and an eosinophilic alveolitis. The pulmonary and systemic symptoms promptly resolved after discontinuation of minocycline.

Effect of an experimental rhinovirus 16 infection on airway mediator response to antigen

Viral respiratory infections provoke wheezing in many patients with asthma. It is our hypothesis that viral respiratory infections enhance the airway inflammatory response to antigen, thus provoking i