title: Eosinophil and T cell markers predict functional decline in COPD patients.
abstract: BACKGROUND
  The major marker utilized to monitor COPD patients is forced expiratory volume in one second (FEV1). However, a single measurement of FEV1 cannot reliably predict subsequent decline. Recent studies indicate that T lymphocytes and eosinophils are important determinants of disease stability in COPD. We therefore measured cytokine levels in the lung lavage fluid and plasma of COPD patients in order to determine if the levels of T cell or eosinophil related cytokines were predictive of the future course of the disease.
  
  
  METHODS
  Baseline lung lavage and plasma samples were collected from COPD subjects with moderately severe airway obstruction and emphysematous changes on chest CT. The study participants were former smokers who had not had a disease exacerbation within the past six months or used steroids within the past two months. Those subjects who demonstrated stable disease over the following six months (DeltaFEV1 % predicted = 4.7 +/- 7.2; N = 34) were retrospectively compared with study participants who experienced a rapid decline in lung function (DeltaFEV1 % predicted = -16.0 +/- 6.0; N = 16) during the same time period and with normal controls (N = 11). Plasma and lung lavage cytokines were measured from clinical samples using the Luminex multiplex kit which enabled the simultaneous measurement of several T cell and eosinophil related cytokines.
  
  
  CONCLUSIONS
  Stable COPD participants had significantly higher plasma IL-2 levels compared to participants with rapidly progressive COPD (p = 0.04). In contrast, plasma eotaxin-1 levels were significantly lower in stable COPD subjects compared to normal controls (p < 0.03). In addition, lung lavage eotaxin-1 levels were significantly higher in rapidly progressive COPD participants compared to both normal controls (p < 0.02) and stable COPD participants (p < 0.05).
  
  
  CONCLUSIONS
  These findings indicate that IL-2 and eotaxin-1 levels may be important markers of disease stability in advanced emphysema patients. Prospective studies will need to confirm whether measuring IL-2 or eotaxin-1 can identify patients at risk for rapid disease progression.
authors.affiliation: Department of Medicine, Columbia University, New York, NY, USA. jmd12@columbia.edu
authors.forename: Jeanine M
authors.initials: JM
authors.lastname: D'Armiento
authors.forename: Steven M
authors.initials: SM
authors.lastname: Scharf
authors.forename: Michael D
authors.initials: MD
authors.lastname: Roth
authors.forename: John E
authors.initials: JE
authors.lastname: Connett
authors.forename: Andrew
authors.initials: A
authors.lastname: Ghio
authors.forename: David
authors.initials: D
authors.lastname: Sternberg
authors.forename: Jonathan G
authors.initials: JG
authors.lastname: Goldin
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Louis
authors.forename: Jenny T
authors.initials: JT
authors.lastname: Mao
authors.forename: George T
authors.initials: GT
authors.lastname: O'Connor
authors.forename: Joe W
authors.initials: JW
authors.lastname: Ramsdell
authors.forename: Andrew L
authors.initials: AL
authors.lastname: Ries
authors.forename: Neil W
authors.initials: NW
authors.lastname: Schluger
authors.forename: Frank C
authors.initials: FC
authors.lastname: Sciurba
authors.forename: Melissa A
authors.initials: MA
authors.lastname: Skeans
authors.forename: Helen
authors.initials: H
authors.lastname: Voelker
authors.forename: Robert E
authors.initials: RE
authors.lastname: Walter
authors.forename: Christine H
authors.initials: CH
authors.lastname: Wendt
authors.forename: Gail G
authors.initials: GG
authors.lastname: Weinmann
authors.forename: Robert A
authors.initials: RA
authors.lastname: Wise
authors.forename: Robert F
authors.initials: RF
authors.lastname: Foronjy
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D018893:Bronchoalveolar Lavage; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D001999:Bronchoscopy; D054413:Chemokine CCL11 / Q000097:blood; D016207:Cytokines / Q000097:blood*; D018450:Disease Progression; D004804:Eosinophils / Q000276:immunology*; D005541:Forced Expiratory Volume; D006801:Humans; D007376:Interleukin-2 / Q000097:blood; D008168:Lung / Q000187:drug effects / Q000276:immunology* / Q000503:physiopathology; D008875:Middle Aged; D011237:Predictive Value of Tests; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D016032:Randomized Controlled Trials as Topic; D019141:Respiratory System Agents / Q000627:therapeutic use; D012189:Retrospective Studies; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000276:immunology*; D013997:Time Factors; D014212:Tretinoin / Q000627:therapeutic use; D014797:Vital Capacity
chemical_list: D015415:Biomarkers; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D016207:Cytokines; C508594:IL2 protein, human; D007376:Interleukin-2; D019141:Respiratory System Agents; D014212:Tretinoin