Bronchial biopsies obtained from 16 asthmatic patients and six normal subjects were analyzed by immunohistochemistry. In the asthmatic patients, the total numbers of macrophages infiltrating the airway mucosa were increased. Many of the macrophages had the phenotypic characteristics of blood monocytes. HLA Class II antigen was expressed on infiltrating cells and airway epithelial cells. In biopsies from the asthmatics there was a significant increase in activated eosinophils, but not in neutrophils. There was also a significant increase in the numbers of T-lymphocytes in the asthmatics, but very few B-lymphocytes were detected. These results suggest that lung macrophages may have a central role to play in the mechanisms of the chronic immune-mediated inflammatory response seen in the airway mucosa of asthmatic patients.

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The pathology of bronchial asthma demonstrates a multicellular process. In an attempt to elucidate the cellular biology of airways inflammation, it becomes important to understand not only the biology of each individual cell type but also the interaction between different cells. This review focuses on a documentation of some of the biological effects of the constituent cells in the airway mucosa and a discussion of their potential interactions through the release and action of different cytokines. It seems likely that future research will address the in vivo release of different cytokine molecules in the asthmatic process using techniques of molecular biology. There likely will be increasing information available about the regulation and the actions of these molecules on target cells and tissues. Elucidation of some of the complex interactions between different cells and the role of different cytokine molecules may provide a novel approach to the therapy of bronchial asthma.