3 research outputs found
Eosinophils in the bronchial mucosa in relation to methacholine dose-response curves in atopic asthma
Asthma is characterized by both local infiltration of eosinophils in the
bronchial mucosa and bronchial hyperreactivity (BHR). A detailed
characterization of BHR implies analysis of a histamine or methacholine
dose-response curve yielding not only the dose at 20% fall of baseline
forced expiratory volume in 1 s (FEV1), but also a plateau (P)
representing the maximal narrowing response in terms of percent change in
FEV1 and reactivity as the steepest slope at 50% of P (%FEV1/doubling
dose). In the baseline condition, the specific airway conductance (sGaw)
may be considered closely related to airway lumen diameter. In 20
nonsmoking asthmatic patients, methacholine dose-response curves were
obtained, and a sigmoid model fit yielded the BHR indexes.
Immunohistochemistry with the monoclonal antibodies (EG1 and EG2) was used
to recognize the total number of eosinophils and activated eosinophils,
respectively. The number of activated eosinophils was significantly
correlated to both P (r = 0.62; P < 0.05) and sGaw (r = -0.52; P < 0.05),
whereas weaker and nonsignificant correlations were found for dose at 20%
fall of baseline FEV1 and the total number of eosinophils. We conclude
that the number of activated eosinophils can be considered a marker of the
inflammation-induced decrease of airway lumen diameter as represented by
the plateau index and sGaw
Increased numbers of dendritic cells in the bronchial mucosa of atopic asthmatic patients: Downregulation by inhaled corticosteroids
Background. Dendritic cells (DC) are the most potent antigen-presenting cells (APC) and stimulators of T cells. Dendritic cells are also likely to be essential for the initiation of allergic immune responses in the lung. However, there are not many data on the presence of dendritic cells in the airways of patients with atopic asthma and on the effects of corticosteroid-treatment on such dendritic cells. Objective. We investigated the distribution of dendritic cells in the bronchial epithelium and mucosa of 16 non-smoking atopic asthmatic patients and eight healthy control subjects using detailed immunohistochemistry (CD1a, HLA-DR, L25 as markers for dendritic cells). Methods. Eleven asthmatics were treated for 2.5 years with bronchodilators only and five with bronchodilators and inhaled beclomethasone dipropionate (BDP), 800 μg daily. The patients were randomly sampled from a double-blind multicentre study. Results. There were higher numbers of CD1a+ DC (P = 0.003), L25+ DC (P = 0.002) and HLA-DR expression (P = 0.042) in the bronchial mucosa of asthmatic patients compared with healthy controls. After 2.5 years of treatment, we found a significant increase in flow expiratory volume in 1 second (FEV1) (P = 0.009) and a significant decrease in hyperresponsiveness (PC20 histamine) (P = 0.013) in the corticosteroid group (n = 5) compared with the bronchodilator group (n = 11). This clinical improvement in the corticosteroid-treated group was accompanied by significantly lower numbers of CD1a+ DC (P=0.008), and HLA-DR expression (P=0.028) in the bronchial mucosa than in the bronchodilator-treated group. Conclusion. Our data suggest that dendritic cells are involved in asthmatic inflammation and that corticosteroids may downregulate the number of dendritic