In the schema of the introductory comments, the reduction in AHR with higher doses of ICS appears targeted to the persistent, or structural, components of AHR. This, however, still remains conjectural. These data also raise the question of how much inflammation, reflected by the presence of eosinophils, contributes to AHR.
To further explore the role of cellular and tissue inflammation, Gibson and colleagues enrolled 20 patients with asthma in a study. Each subject was given 2,000 mg of beclomethasone per day for 8 weeks. At the completion of this treatment phase, AHR was measured to methacholine and hypertonic saline. These determinants of AHR were followed by a collection of induced sputum. One week later, the subjects under went a bronchoscopy with lavage and mucosal biopsy to evaluate airway lumen and mucosal inflammation. The changes in AHR were compared with the various markers of inflammation, including airway lumen and airway wall (Table 1). Changes in AHR to methacholine Canadian online viagra, in particular, were associated with reductions in mucosal (bronchial biopsy) metachromatic cells. In contrast, associated changes in eosinophils had less effect on AHR to methacholine or mannitol.
From these observations, the authors concluded that the effects of reducing cellular inflammation on AHR were dependent upon many factors, including the cell type (ie, eosinophil vs metachromatic cell) and the location of the inflammatory process (ie, the lumen vs airway wall). Under these experimental conditions, two major messages can be drawn: metachromatic cells and their residence in the airway wall are the dominant factors that are most likely to influence altered airway physiology associated with AHR. Their findings also suggest that long-term treatments with effective doses of ICS are needed to bring about changes in the mucosal tissue and for these changes to translate into functional improvement in AHR. This study also underscores the strength behind combining assessments of inflammatory cell type and their location to unravel which cell and under what conditions it affects AHR. Again, this study suggests that it is the structural status of the airway, not necessarily inflammation, that is important to AHR.
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