title: Interleukin-9 receptor expression in asthmatic airways In vivo.
abstract: Inflammation of the airway wall is a defining feature in asthma and is likely the cause of the hyperreactivity and variable airflow limitation found in asthma. Immune response biased toward production of Th2 cytokines has been proposed as a mechanism in the pathogenesis of airway inflammation in asthma. The Th2 cytokine interleukin-9 (IL-9) is one candidate gene for asthma on the basis of position cloning and animal models of airway inflammation. To determine whether IL-9 is involved in the chronic inflammation of the asthmatic airway, we investigated the expression of IL-9 and the IL-9 specific receptor chain in asthmatic airways compared with healthy airways. IL-9 and IL-9 receptor expression in airway epithelial cells and bronchoalveolar lavage cells obtained at bronchoscopy of healthy (n = 9) and mild intermittent asthmatic individuals (n = 7) were studied by Northern analyses and reverse-transcription polymerase chain reaction technique. Primary and transformed human airway epithelial cells were also evaluated for IL-9 specific receptor chain expression in vitro. IL-9 was not detected in airways of healthy or mild asthmatic individuals. In contrast, IL-9 specific receptor chain expression was found in asthmatic airway samples but not in healthy controls. In vitro, airway epithelial cells did not express IL-9 specific receptor chain until stimulation with interferon gamma. Our results support that IL-9 may play a role in the mechanism leading to chronic airway inflammation and asthma.
authors.affiliation: Department of Pulmonary and Critical Care Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
authors.forename: P R
authors.initials: PR
authors.lastname: Bhathena
authors.forename: S A
authors.initials: SA
authors.lastname: Comhair
authors.forename: K J
authors.initials: KJ
authors.lastname: Holroyd
authors.forename: S C
authors.initials: SC
authors.lastname: Erzurum
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001249:Asthma / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015415:Biomarkers; D015139:Blotting, Southern; D001980:Bronchi / Q000378:metabolism* / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D001999:Bronchoscopy; D002478:Cells, Cultured; D017931:DNA Primers / Q000737:chemistry; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D006801:Humans; D016906:Interleukin-9 / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D012313:RNA / Q000235:genetics / Q000378:metabolism*; D018123:Receptors, Interleukin / Q000235:genetics / Q000378:metabolism*; D053651:Receptors, Interleukin-9; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
chemical_list: D015415:Biomarkers; D017931:DNA Primers; C508045:IL9R protein, human; D016906:Interleukin-9; D018123:Receptors, Interleukin; D053651:Receptors, Interleukin-9; D012313:RNA