title: [Role of inflammation in the etiopathogenesis of COPD].
abstract: Inflammation is one of the first immune system responses to any type of aggression. As with any type of aggression, the lesion produced by inhalation of tobacco smoke prompts an innate inflammatory response. Subsequently, this lesion is stimulated by the release of various chemical factors that enhance the inflammatory response and, finally--depending on the type of aggression--acquired immunity is activated, which, mediated by lymphocyte participation, serves to establish a physical barrier against the propagation of the lesion and to aid repair of the damaged pulmonary tissue. However, the balance between inflammation and repair is not always maintained, as is the case in chronic obstructive pulmonary disease (COPD), in which marked changes appear in the architecture of the airways, alveolar spaces and pulmonary arteries, forming the structural background of the functional changes characteristic of this disease. COPD is basically a pulmonary disease but data are available on the existence of associated systemic inflammation. The origins of this systemic inflammation are unclear: some information indicates that tobacco smoke is a direct origin common to local and systemic inflammation, while other data point to primary pulmonary inflammation that secondarily produces systemic involvement. The present review describes the main mechanisms involved in both pulmonary and systemic inflammation in COPD.
authors.affiliation: Laboratorio de Neumología Experimental, IIS-Fundación Jiménez Díaz, CIBERES, Madrid, España.
authors.forename: Laura
authors.initials: L
authors.lastname: del Puerto-Nevado
authors.forename: Sandra
authors.initials: S
authors.lastname: Pérez-Rial
authors.forename: Alvaro
authors.initials: A
authors.lastname: Girón-Martínez
authors.forename: Germán
authors.initials: G
authors.lastname: Peces-Barba
mesh_terms: D056151:Airway Remodeling; D017209:Apoptosis; D018925:Chemokines / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D005340:Fibrinogen / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000502:physiology; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D016131:Lymphocyte Subsets / Q000276:immunology; D008264:Macrophages / Q000502:physiology; D008954:Models, Biological; D009504:Neutrophils / Q000502:physiology; D018384:Oxidative Stress; D010447:Peptide Hydrolases / Q000502:physiology; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D012906:Smoke / Q000009:adverse effects
chemical_list: D018925:Chemokines; D016207:Cytokines; D018836:Inflammation Mediators; D036341:Intercellular Signaling Peptides and Proteins; D012906:Smoke; D005340:Fibrinogen; D010447:Peptide Hydrolases