title: [COPD and inflammation: statement from a French expert group. Phenotypes related to inflammation].
abstract: BACKGROUND
  The objective of the present article is to review available data on possible links between phenotypes and inflammatory profiles in patients with chronic obstructive pulmonary disease (COPD).
  
  
  BACKGROUND
  Chronic bronchitis is associated with proximal bronchial inflammation and small airway inflammation with remodeling at the site of obstruction. CT scanning enables patients to be phenotyped according to the predominantly bronchial or emphysematous nature of the morphological abnormality. Exacerbations, in a context of persistently elevated baseline inflammation, are associated with increased inflammation and a poor prognosis. Long-term studies have correlated inflammatory markers (and anti-inflammatory drug effects) with dynamic hyperinflation, possibly confirming that inflammation promotes hyperinflation. The inflammatory cell count in the pulmonary arterial walls correlates with the severity of endothelial dysfunction. The risk of developing pulmonary hypertension would seem to increase with low-grade systemic inflammation. The role of low-grade systemic inflammation in COPD co-morbidities, and in nutritional and muscular involvement in particular, remains a matter of debate. Regular physical exercise may help reduce this inflammation.
  
  
  CONCLUSIONS
  In COPD, many aspects of the clinical phenotype are related to inflammation. Better knowledge of these relationships could help optimize current and future treatments.
authors.affiliation: Service de pneumologie et immuno-allergologie, hôpital Calmette, CHRU de Lille, boulevard du Professeur-J.-Leclercq, Lille, France. thierry.perez@chru-lille.fr
authors.forename: T
authors.initials: T
authors.lastname: Perez
authors.forename: H
authors.initials: H
authors.lastname: Mal
authors.forename: B
authors.initials: B
authors.lastname: Aguilaniu
authors.forename: P-Y
authors.initials: PY
authors.lastname: Brillet
authors.forename: A
authors.initials: A
authors.lastname: Chaouat
authors.forename: R
authors.initials: R
authors.lastname: Louis
authors.forename: J-F
authors.initials: JF
authors.lastname: Muir
authors.forename: T
authors.initials: T
authors.lastname: Similowski
authors.forename: P
authors.initials: P
authors.lastname: Berger
authors.forename: P-R
authors.initials: PR
authors.lastname: Burgel
authors.forename: A
authors.initials: A
authors.lastname: Chambellan
authors.forename: P
authors.initials: P
authors.lastname: Chanez
authors.forename: P
authors.initials: P
authors.lastname: Devillier
authors.forename: R
authors.initials: R
authors.lastname: Escamilla
authors.forename: R
authors.initials: R
authors.lastname: Marthan
authors.forename: B
authors.initials: B
authors.lastname: Wallaert
authors.forename: M
authors.initials: M
authors.lastname: Aubier
authors.forename: N
authors.initials: N
authors.lastname: Roche
mesh_terms: D001991:Bronchitis / Q000150:complications; D002908:Chronic Disease; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology; D007249:Inflammation / Q000150:complications / Q000235:genetics*; D010641:Phenotype; D011379:Prognosis; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology; D011656:Pulmonary Emphysema / Q000150:complications; D012720:Severity of Illness Index; D012907:Smoking / Q000009:adverse effects