title: Airway inflammation in patients with chronic non-asthmatic cough.
abstract: BACKGROUND
  Chronic non-asthmatic cough (CC) is a clinical challenge and underlying pathophysiological mechanisms remain still not completely understood. One of the most common comorbidities in CC is gastro-oesophageal reflux disease (GORD). Airway epithelium damage can contribute to airway inflammation in CC.
  
  
  OBJECTIVE
  We studied airway inflammation in patients with CC compared to healthy controls. Patients with GORD were treated with proton pump inhibitors (PPI) and cough response to PPI was evaluated.
  
  
  METHODS
  Sputum was induced in 41 adults with CC and 20 healthy non-smokers who were age and sex matched. We compared sputum differential cell count by cytospin and cytokine and chemokine production at the mRNA and/or protein levels by real-time (RT)-PCR and cytokine bead array (CBA), between patients with CC and healthy subjects. Furthermore we studied airway inflammation in patients with different comorbidities.
  
  
  RESULTS
  No differences in sputum differential cell counts were observed between patients with CC and healthy subjects. Sputum monocyte chemoattractant protein-1 (MCP-1) protein levels were significantly higher in patients when compared to controls. Thymic stromal lymphopoietin (TSLP) mRNA was significantly more often expressed in sputum of patients with CC than from healthy controls. Sputum transforming growth factor (TGF)-β levels did not differ between patients and controls, but were significantly lower in the PPI responders compared to the non-responders; p=0.047. There is no evidence for impaired T helper cell (Th)1/Th2/Th17 balance in CC. Patients with reflux oesophagitis (RO) have significantly more sputum eosinophils than patients without RO.
  
  
  CONCLUSIONS
  CC is a condition presenting with different disease phenotypes. High sputum MCP-1 levels are present in a large group of patients with CC and a majority of these patients with CC have increased sputum TSLP levels, most likely produced by damaged airway epithelial cells.
authors.affiliation: Department of Physiology, Wroclaw Medical University, Wroclaw, Poland. marcingrabow@o2.pl
authors.forename: Marcin
authors.initials: M
authors.lastname: Grabowski
authors.forename: Sven
authors.initials: S
authors.lastname: Seys
authors.forename: Ann
authors.initials: A
authors.lastname: Decraene
authors.forename: Ahmad
authors.initials: A
authors.lastname: Kasran
authors.forename: Ellen
authors.initials: E
authors.lastname: Dilissen
authors.forename: Wojciech
authors.initials: W
authors.lastname: Barg
authors.forename: Wojciech
authors.initials: W
authors.lastname: Medrala
authors.forename: Lieven J
authors.initials: LJ
authors.lastname: Dupont
authors.forename: Bernard
authors.initials: B
authors.lastname: Panaszek
authors.forename: Dominique M A
authors.initials: DM
authors.lastname: Bullens
mesh_terms: D000328:Adult; D001980:Bronchi / Q000473:pathology; D001991:Bronchitis / Q000453:epidemiology* / Q000473:pathology; D002452:Cell Count; D018932:Chemokine CCL2 / Q000032:analysis; D015897:Comorbidity; D003371:Cough / Q000453:epidemiology* / Q000235:genetics / Q000473:pathology; D016207:Cytokines / Q000032:analysis; D005260:Female; D005764:Gastroesophageal Reflux / Q000188:drug therapy / Q000453:epidemiology; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D054328:Proton Pump Inhibitors / Q000627:therapeutic use; D013183:Sputum / Q000166:cytology / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000032:analysis; D000094632:Thymic Stromal Lymphopoietin
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D016207:Cytokines; D054328:Proton Pump Inhibitors; D016212:Transforming Growth Factor beta; D000094632:Thymic Stromal Lymphopoietin