title: Systemic inflammation and COPD: the Framingham Heart Study.
abstract: BACKGROUND
  The current paradigm for the pathogenesis of COPD includes an ultimately maladaptive local inflammatory response to environmental stimuli. We examined the hypothesis that systemic inflammatory biomarkers are associated with impaired lung function, particularly among those with extensive cigarette smoking.
  
  
  METHODS
  Using data from the Framingham Heart Study, we examined cross-sectional associations of systemic inflammatory biomarkers (CD40 ligand [CD40L], intercellular adhesion molecule [ICAM]-1, interleukin [IL]-6, monocyte chemoattractant protein-1, P-selectin, and myeloperoxidase, in addition to C-reactive protein) to impaired lung function.
  
  
  RESULTS
  IL-6 was consistently associated with impaired lung function; a 1-SD higher concentration of IL-6 was associated with a 41-mL lower FEV(1) (95% confidence interval [CI], - 61 to - 20) and a borderline 15% higher odds of COPD (odds ratio, 1.15; 95% CI, 0.99 to 1.34). Additionally, P-selectin was associated with lower FEV(1) levels; after adjusting for the other biomarkers, a 1-SD higher concentration of P-selectin predicted an FEV(1) that was on average 19 mL lower (95% CI, - 37 to 0). Including the biomarkers individually as sole exposures in the models generally strengthened the impaired lung function/biomarker association; the relations of ICAM-1 to FEV(1), and ICAM and CD40L to COPD became significant. The observed associations did not vary significantly with smoking history, except that the association between CD40L and COPD appeared greater in individuals with more extensive smoking histories.
  
  
  CONCLUSIONS
  Among participants in the Framingham Heart Study, systemic inflammation was associated with lower levels of pulmonary function. Further research into the role of systemic inflammation in the development of pulmonary dysfunction is merited.
authors.affiliation: Section of Pulmonary, Allergy, and Critical Care Medicine, Boston University School of Medicine, Boston, MA 02118, USA. walterb@bu.edu
authors.forename: Robert E
authors.initials: RE
authors.lastname: Walter
authors.forename: Jemma B
authors.initials: JB
authors.lastname: Wilk
authors.forename: Martin G
authors.initials: MG
authors.lastname: Larson
authors.forename: Ramachandran S
authors.initials: RS
authors.lastname: Vasan
authors.forename: John F
authors.initials: JF
authors.lastname: Keaney
authors.forename: Izabella
authors.initials: I
authors.lastname: Lipinska
authors.forename: George T
authors.initials: GT
authors.lastname: O'Connor
authors.forename: Emelia J
authors.initials: EJ
authors.lastname: Benjamin
mesh_terms: D015415:Biomarkers / Q000097:blood; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000150:complications*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology
chemical_list: D015415:Biomarkers