When cellular inflammation was determined by BAL eosinophils

These studies were then repeated 7 days after the allergen challenge to assess the persistence of the inflammatory reaction and to determine whether the inflammatory changes associated with changes in AHR were in the airway lumen, bronchial mucosa inflammation, or both.

Twenty-four hours after allergen challenge, there was, as expected, a significant decrease in the FEVin the majority of patients. Furthermore, AHR to methacholine increased at 24 h post allergen challenge and remained increased at 7 days (Fig 8). When cellular inflammation was determined by BAL eosinophils, a significant increase in this cell was found 24 h after allergen challenge; however, by 7 days post allergen challenge, the eosinophils in the BAL had returned to baseline levels buy Viagra Australia. In contrast, when the investigators measured procollagen-expressing cells in the bronchial biopsy specimen as a marker of airway remodeling, there was an increase in this mucosal marker 7 days after allergen challenge (Fig 9). These data suggest that the changes in AHR following allergen challenge appear to be more closely associated with structural alterations than the early recruitment of luminal eosinophils and ensuing inflammation. Although eosinophils tend to parallel these responses, they did not appear to be the causative process in this response.

Assessing the contribution to airway inflammatory events to AHR is complicated by many factors, includ-ing the method of evaluation, the measurement itself, the timing of the readout, and the susceptibility to the inflammatory determinant. For example, detection of airway inflammation is facilitated by noninvasive approaches, such as analysis of induced sputum samples. These determinants measure events in the large to midsize airways. Bronchoscopy with lavage, in contrast, provides a “cleaner” sample but requires an invasive procedure, which by itself can have effects on markers of inflammation. Both sputum and lavage samples reflect inflammation in the airway lumen, which may not fully reflect the histology of the airway wall, a location that is more likely to be a determinant of AHR.

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