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Related Articles Effect of salmeterol/fluticasone propionate on airway inflammation in COPD:a randomized controlled trial. Thorax. 2007 Jun 8; Authors: Bourbeau J, Christodoulopoulos P, Maltais F, Yamauchi Y, Olivenstein R, Hamid Q Airway inflammation in chronic obstructive pulmonary disease (COPD) is characterized by infiltration of CD8+ T cells and CD68+ macrophages and an increased number of neutrophils, whereas few studies have described the presence of eosinophils. Although anti-inflammatory effects of corticosteroids in stable COPD are unclear, recent studies suggest that combination therapy could be beneficial. We therefore evaluated combined salmeterol/fluticasone propionate (SFC) and fluticasone propionate (FP) alone on inflammatory cells in the airways of COPD patients. Patients were treated in a randomized, double-blind, parallel-group, placebo-controlled trial with either a combination of 50microg salmeterol and 500microg FP twice daily ([SFC] n=19, 19 male, mean age 62), 500microg FP twice daily (n=20, 15 male, mean age 64), or placebo (n=21, 17 male, mean age 66) for 3 months. At the start and end of treatment, bronchoscopy with bronchial biopsies was performed, and numbers of CD8+ T lymphocytes, CD68+ macrophages, neutrophils and eosinophils were measured. CD8+ cells were significantly reduced by SFC compared with placebo (difference -98.05 cells/mm2; 95% CI -143.14 to -52.9; p<0.001). Such a marked effect was not seen with FP alone (-44.67 cells/mm2; 95% CI -90.92 to 1.57; p=0.06). CD68+ macrophages were also reduced by SFC compared with placebo (difference -31.68 cells/mm2; 95% CI -61.07 to -2.29; p=0.03) but not by FP. SFC did not significantly change neutrophils and eosinophils compared with placebo. SFC has airway anti-inflammatory effects not seen with inhaled corticosteroids alone.
Related Articles Symposium on obesity and asthma - November 2, 2006. Can Respir J. 2007 May-Jun;14(4):201-8 Authors: Boulet LP, Hamid Q, Bacon SL, Bergeron C, Boulet LP, Chen Y, Dixon AE, Ernst P, Hamid Q, Holguin F, Irvin CG, Kimoff RJ, Komakula S, Laprise C, Lavoie KL, Shore SA, Teodorescu M, Vohl MC Asthma and obesity are frequently associated, and obesity has been considered a factor contributing to both an increase in severity of asthma and to its development. The present document summarizes the proceedings of a symposium held in Montreal, Quebec, on November 2, 2006, under the auspices of the Réseau en santé respiratoire du Fonds de la recherche en santé du Québec in collaboration with the McGill University -- Strauss Severe Asthma Program, Université Laval (Quebec City) and Université de Montréal. It includes an overview of the various aspects of the relationships between asthma and obesity with regard to animal models; genetic, hormonal and physiological determinants; influence of comorbidities (eg, sleep apnea syndrome); epidemiology; clinical and psychological features; and management of asthma in the obese population.
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Related Articles Increased expression of ADAM33 and ADAM8 with disease progression in asthma. J Allergy Clin Immunol. 2007 Mar 3; Authors: Foley SC, Mogas AK, Olivenstein R, Fiset PO, Chakir J, Bourbeau J, Ernst P, Lemière C, Martin JG, Hamid Q BACKGROUND: ADAM33, a disintegrin and metalloproteinase 33 gene, has been identified as a risk factor for asthma and bronchial hyperresponsiveness and has been postulated as a gene for airway remodeling. ADAM8 is strongly induced by allergens and T(H)2 cytokines in the lung in experimental asthma. OBJECTIVES: To assess the importance of these genes in asthma pathogenesis and to investigate whether expression relates to disease severity or deterioration in lung function, we measured the mRNA and protein expression of both genes in bronchial biopsies of subjects with asthma and control subjects. METHODS: RNA was extracted from frozen endobronchial biopsies of mild, moderate, and severe adults with asthma and controls. Subjects with moderate and severe asthma were taking corticosteroids. The mRNA transcript of both genes was measured by real time RT-PCR using specific primers. Protein expression was examined by immunohistochemistry on paraffin sections. RESULTS: ADAM33 mRNA expression was significantly higher in both moderate and severe asthma compared with mild asthma (P < .05) and controls. Immunostaining for ADAM33 was increased in the epithelium, submucosal cells, and smooth muscle in severe asthma compared with mild disease and controls. ADAM8 mRNA expression was significantly increased in all asthma groups compared with controls. Increased inflammatory cells stained positive for ADAM8 in both moderate (P < .05) and severe asthma (P < .005) compared with mild disease. CONCLUSIONS: These results demonstrate increased expression of both ADAM genes as asthma severity increases. CLINICAL IMPLICATIONS: These genes may contribute to the remodeling process that occurs with asthma progression and may have implications for future treatment in severe disease.
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Related Articles Influence of cigarette smoke on the arginine pathway in asthmatic airways: Increased expression of arginase I. J Allergy Clin Immunol. 2007 Feb;119(2):391-7 Authors: Bergeron C, Boulet LP, Page N, Laviolette M, Zimmermann N, Rothenberg ME, Hamid Q BACKGROUND: Up to 30% of asthmatic subjects are smokers, and smoking might be an important contributor to asthma pathology. Inducible nitric oxide synthase (iNOS), ornithine decarboxylase (ODC), and arginase I are involved in the arginine pathway. We have shown that arginase I and iNOS are upregulated in asthma. Smoking asthmatic subjects are reported to have low exhaled nitric oxide levels. The effect of cigarette smoking on the expression of arginase I in asthma is unknown. OBJECTIVES: The aims of this study were to investigate the expression of arginase I, ODC, and iNOS in asthmatic airways of smokers and nonsmokers and in vitro after nicotine stimulation. METHODS: Endobronchial biopsies were performed on 24 steroid-naive subjects with mild asthma: 12 smokers and 12 nonsmokers. Arginase I, ODC, and iNOS levels were assessed by means of immunohistochemistry and in situ hybridization (arginase I). In vitro stimulation of airway cells with nicotine was performed, followed by real-time PCR. RESULTS: Arginase I, ODC, and iNOS were expressed in the epithelium and smooth muscle bundles of both subgroups of asthmatic subjects. There was an increase of arginase I and ODC immunoreactivities in smoking compared with nonsmoking asthmatic subjects. There was no significant difference in immunoreactivity for iNOS between groups. Nicotine induced a 2-fold increase in arginase I and ODC expression in airway epithelial cells and fibroblasts. CONCLUSION: This study demonstrates that the expression of arginase I and ODC is increased in airways of smoking compared with nonsmoking asthmatic subjects and in vitro by nicotine. CLINICAL IMPLICATIONS: Increased expression of arginase I might lead to low exhaled nitric oxide and chronic obstructive pulmonary disease-like airway remodeling in smoking asthmatic subjects.
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