title: Neutrophil adhesion molecules in experimental rhinovirus infection in COPD.
abstract: BACKGROUND
  COPD exacerbations are associated with neutrophilic airway inflammation. Adhesion molecules on the surface of neutrophils may play a key role in their movement from blood to the airways. We analysed adhesion molecule expression on blood and sputum neutrophils from COPD subjects and non-obstructed smokers during experimental rhinovirus infections.
  
  
  METHODS
  Blood and sputum were collected from 9 COPD subjects and 10 smoking and age-matched control subjects at baseline, and neutrophil expression of the adhesion molecules and activation markers measured using flow cytometry. The markers examined were CD62L and CD162 (mediating initial steps of neutrophil rolling and capture), CD11a and CD11b (required for firm neutrophil adhesion), CD31 and CD54 (involved in neutrophil transmigration through the endothelial monolayer) and CD63 and CD66b (neutrophil activation markers). Subjects were then experimentally infected with rhinovirus-16 and repeat samples collected for neutrophil analysis at post-infection time points.
  
  
  RESULTS
  At baseline there were no differences in adhesion molecule expression between the COPD and non-COPD subjects. Expression of CD11a, CD31, CD62L and CD162 was reduced on sputum neutrophils compared to blood neutrophils. Following rhinovirus infection expression of CD11a expression on blood neutrophils was significantly reduced in both subject groups. CD11b, CD62L and CD162 expression was significantly reduced only in the COPD subjects. Blood neutrophil CD11b expression correlated inversely with inflammatory markers and symptom scores in COPD subjects.
  
  
  CONCLUSIONS
  Following rhinovirus infection neutrophils with higher surface expression of adhesion molecules are likely preferentially recruited to the lungs. CD11b may be a key molecule involved in neutrophil trafficking in COPD exacerbations.
authors.affiliation: Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, Norfolk Place, London W2 1PG, UK.
authors.forename: Patrick
authors.initials: P
authors.lastname: Mallia
authors.forename: Simon D
authors.initials: SD
authors.lastname: Message
authors.forename: Marco
authors.initials: M
authors.lastname: Contoli
authors.forename: Katrina K
authors.initials: KK
authors.lastname: Gray
authors.forename: Aurica
authors.initials: A
authors.lastname: Telcian
authors.forename: Vasile
authors.initials: V
authors.lastname: Laza-Stanca
authors.forename: Alberto
authors.initials: A
authors.lastname: Papi
authors.forename: Luminita A
authors.initials: LA
authors.lastname: Stanciu
authors.forename: Sarah
authors.initials: S
authors.lastname: Elkin
authors.forename: Onn M
authors.initials: OM
authors.lastname: Kon
authors.forename: Malcolm
authors.initials: M
authors.lastname: Johnson
authors.forename: Sebastian L
authors.initials: SL
authors.lastname: Johnston
mesh_terms: D000328:Adult; D000368:Aged; D015815:Cell Adhesion Molecules / Q000276:immunology*; D002478:Cells, Cultured; D003139:Common Cold / Q000276:immunology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology*; D012907:Smoking / Q000276:immunology*
chemical_list: D015815:Cell Adhesion Molecules