Activation of Pulmonary Mast Cells by Bronchoalveolar Allergen Challenge:In VivoRelease of Histamine and Tryptase in Atopic Subjects with and without Asthma

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Abstract
Human mast cells likely play a significant role in human asthma. In the present study, concentrations of tryptase and histamine in bronchoalveolar lavage fluid (BALF) were used as indicators of pulmonary mast cell activation. BALF was obtained before and after endobronchial allergen challenge and assessed for mediator content and cell composition in 4 subject groups: nonatopic nonasthmatics (Group 1, n = 7), nonatopic asthmatics (Group 2, n = 3), atopic nonasthmatics (Group 3, n = 7), and atopic asthmatics (Group 4, n = 7). Before challenge, histamine concentrations were not different between the 4 groups, whereas tryptase concentrations were significantly greater in the atopic asthmatics than in each of the other groups (p < 0.04). Allergen challenge in atopic asthmatics resulted in significant increases above baseline in mean ± SD histamine (0.7 ± 7.1 to 2.8 ± 2.0 ng/ml) and tryptase (2.0 ± 1.7 to 10.1 ± 8.2 ng/ml) concentrations in BALF (p < 0.03). Atopic nonasthmatics also had increases above baseline in histamine (0.2 ± 0.2 to 1.2 ± 1.4 ng/ml) and tryptase (0.5 ± 0.4 to 1.4 ± 1.03 ng/ml) concentrations after allergen challenge (p < 0.05). Though the histamine values were not significantly different between atopic nonasthmatics and atopic asthmatics after allergen challenge, tryptase concentrations were markedly higher in the atopic asthmatic group. The numbers, as well as the predominance of the T mast cell type in atopic asthmatics and nonasthmatics, were no different from controls. In nonatopic subjects, regardless of asthmatic state, histamine or tryptase concentrations were not altered by allergen challenge. Pulmonary mast cell activation occurs after allergen challenge in subjects with atopy and asthma and, to a lesser degree, in those with atopy alone. Activation of these cells at baseline in the atopic asthmatic group implicates mast cell involvement in the persistence of the asthmatic state in these individuals.