CHRONIC COUGH RESEMBLES ASTHMA WITH IL-5 AND GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR GENE-EXPRESSION IN BRONCHOALVEOLAR CELLS

Background: Chronic cough is a multifactorial condition, which, like a sthma, can be associated with eosinophilic air-way inflammation, In as thma, airway eosinophilia is believed to be mediated by cytokines such as interleukin-5 and granulocyte macrophage colony stimulating: facto r (GM-CSF). The role of these cytokines in chronic cough is unclear. O bjective: The aim of this study this to examine gene expression for IL -5 and GM-CSF in chronic cough and compare the results with those foun d in asthma. Methods: We studied adults with asthma (n = 12), chronic cough responsive to inhaled corticosteroid (ICS-responsive cough) (n = 9), and chronic cough not responsive to inhaled corticosteroid (non-I CS-responsive cough) (n = 4). Bronchoalveolar lavage (BAL) was perform ed and cytokine gene expression was assessed by using a semiquantitati ve reverse transcriptase polymerase chain reaction. Results: IL-5 mRNA was expressed by BAL cells from nine of 12 asthmatic subjects and six of nine subjects with ICS-responsive chronic cough. IL-5 mRNA was not detected in subjects with non-ICS-responsive chronic cough (zero of f our subjects, p < 0.05). GM-CSF mRNA was expressed in BAL cells from s even of 12 asthmatic subject's and six of nine subjects with ICS-respo nsive cough. GM-CSF mRNA was not detected in non-ICS responsive cough subjects (zero of four subjects, p < 0.05). GM-CSF gene expression was related to the degree of methacholine airway responsiveness in asthma tic subjects (r = -0.59). Conclusion: We conclude that chronic cough, like asthma, if associated with airway inflammation and gene expressio n for IL-5 and GM-CSF. Ongoing expression of these cytokines is likely to be related to the persistence of airway inflammation and chronic c ough.