Airway Inflammation and the Pathogenesis of Asthma
Airway inflammation has been recognized for more than l00 years to be present in the airways of patients with severe asthma. Much more recently, airway intlammation has been identified to be central to the pathogenesis of all asthma. The inflammation is of a characteristic type, with the presence of...
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| Main Author: | |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1994-01-01
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| Series: | Canadian Respiratory Journal |
| Online Access: | http://dx.doi.org/10.1155/1994/767528 |
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| Summary: | Airway inflammation has been recognized for more than
l00 years to be present in the airways of patients with severe
asthma. Much more recently, airway intlammation has been
identified to be central to the pathogenesis of all asthma.
The inflammation is of a characteristic type, with the presence
of activated eosinophils, mast cells and lymphocytes
in bronchoalveolar lavage fluid and airway biopsies from
patients with even mild asthma. Stimuli that are known to
worsen asthma, such as inhaled allergens, also increase the
numbers of mast cells and cosinophils in asthmatic airways.
In addition, treatment with inhaled corticoteroids - the
most effective treatment for asthma - improves symptoms
and reduces the numbers of eosinophil s, mast cells and
lymphocytes in the airways. The precise functions of the
cells in promoting inflammation and causing asthma symptoms
has not yet been fully elucidated. However, it is very
likely that eicosanoids, such as the cysteinyl leukotrienes,
are produced by eosinophils and mast cells and are a major
cause of bronchoconstriction in asthma. Also, these inflammatory
cells can produce proinflammatory cytokines,
such as granulocytc-macrophage colony-stimulating factor.
interleukin (IL) 3 and IL-5, which may promote continuing
inflammation in the airways. Lastly, the persisting inflammatory
cell infiltrate and products re leased from these cells
arc very likely the cause or the airway structural changes
characteristic of asthma, such as epithelial damage, goblet
cell hyperplasia. smooth muscle thickening and deposition
of collagen below the basement membrane. These changes
have been suggested tn he the cause of airway hyperresponsiveness
in asthma. An improved understanding of the precise
mechanisms by which airway inflammation is initiated,
propagates and causes airway damage will hopefully allow
more precise treatment strategies to he developed for
asthma than currently exist. |
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| ISSN: | 1198-2241 |