title: [COPD and inflammation: statement from a French expert group: inflammation and remodelling mechanisms].
abstract: The present study reviews the literature on inflammation and remodelling mechanisms in chronic obstructive pulmonary disease (COPD). The development of COPD is associated with chronic pulmonary inflammation. Immunity (innate or adaptive) plays a role in its onset and continuation. Airways inflammation alters bronchial structure/function relations: increased bronchial wall thickness, increased bronchial smooth muscle tone, seromucosal gland hypersecretion and loss of elastic structures. Circulating markers of pulmonary inflammation indicate its systemic dissemination. Oxidative stress plays a major role in the onset and persistence of tissue abnormalities. The determinants of extra- and intra-cellular redox control are only partially known. Susceptibility genes, antioxidant system insufficiency and reduced levels of anti-age molecules and of histone deacetylation are also involved. The molecular and cellular targets of inflammation and remodelling are numerous and complex. Currently, tools exist to limit inflammation in COPD but not to act on structural remodelling.
authors.affiliation: Inserm U 700, Service de Pneumologie A, Hôpital Bichat-Claude-Bernard, Groupement Hospitalier Universitaire Nord, Faculté de Médecine de Paris-Diderot, 46 Rue Henri-Huchard, 75018 Paris 7, France. michel.aubier@bch.aphp.fr
authors.forename: M
authors.initials: M
authors.lastname: Aubier
authors.forename: R
authors.initials: R
authors.lastname: Marthan
authors.forename: P
authors.initials: P
authors.lastname: Berger
authors.forename: A
authors.initials: A
authors.lastname: Chambellan
authors.forename: P
authors.initials: P
authors.lastname: Chanez
authors.forename: B
authors.initials: B
authors.lastname: Aguilaniu
authors.forename: P-Y
authors.initials: PY
authors.lastname: Brillet
authors.forename: P-R
authors.initials: PR
authors.lastname: Burgel
authors.forename: A
authors.initials: A
authors.lastname: Chaouat
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: Louis
authors.forename: H
authors.initials: H
authors.lastname: Mal
authors.forename: J-F
authors.initials: JF
authors.lastname: Muir
authors.forename: T
authors.initials: T
authors.lastname: Pérez
authors.forename: T
authors.initials: T
authors.lastname: Similowski
authors.forename: B
authors.initials: B
authors.lastname: Wallaert
authors.forename: N
authors.initials: N
authors.lastname: Roche
mesh_terms: D056151:Airway Remodeling / Q000276:immunology / Q000502:physiology*; D000740:Anemia / Q000453:epidemiology / Q000209:etiology; D000941:Antigens / Q000009:adverse effects / Q000276:immunology; D000975:Antioxidants / Q000627:therapeutic use; D001991:Bronchitis / Q000150:complications / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000453:epidemiology; D015897:Comorbidity; D016207:Cytokines / Q000502:physiology; D003713:Dendritic Cells / Q000276:immunology; D048909:Diabetes Complications / Q000453:epidemiology / Q000209:etiology; D004548:Elasticity; D020022:Genetic Predisposition to Disease; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D018836:Inflammation Mediators; D008954:Models, Biological; D009093:Mucus / Q000378:metabolism; D009129:Muscle Tonus; D009130:Muscle, Smooth / Q000503:physiopathology; D010024:Osteoporosis / Q000453:epidemiology / Q000209:etiology; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology
chemical_list: D000941:Antigens; D000975:Antioxidants; D016207:Cytokines; D018836:Inflammation Mediators