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KMID : 0383819950420040431
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Tuberculosis and Respiratory Diseases
1995 Volume.42 No. 4 p.431 ~ p.446
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Pathogenesis of Bronchial Asthma
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Tak H. Lee
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Abstract
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The pathology of bronchial asthma demonstrates a multicellular process. The airway
mucosa is infiltrated with both mononuclear cells and granulocytes, of which the
eosinophil is particularly prominent. In order to attempt an elucidation of the cellular
biology of airways inflammation, it is important to understand both the interactions
between different cells and the biology of each individual cell type. Our work has
focused on the effects of monocyte and macrophage-derived cellular products on
granulocytic and T cell function because of the evidence for monocyte and macrophage
activation in bronchial asthma.
There is enhanced expression of FcεR2 and complement receptors in
peripheral blood monocytes of asthmatic patients and increased expression of complement
receptors as measured by a rosetting technique, in the monocytes of asthmatic patients
after allergen bronchoprovocation. The alveolar macrophages of patients with asthma
demonstrate increased capacity to produce eicosanoid mediators and superoxide anions.
Furthermore, these cells bear FcεR2 on their surface and can be
stimulated to release mediators by IgE-dependent events.
Analysis of bronchoalveolar lavage fluid of patients with asthma after antigen
challenge revealed increased amounts of β-glucuronidase whereas macrophage
intracellular levels were decreased, suggesting that the macrophage secretory processes
were activated by allergen. Furthermore, Metzger has shown that the numbers of
monocytes in the airways increase at 48 hours after antigen provocation in asthmatic
patients.
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