title: [Biopathology of fibrosing alveolitis].
abstract: Fibrosis is a condition where the functional tissue of an organ has been replaced by mesenchymal cells and their extracellular matrix. The process is frequent and may be regarded as univocal and independent of aetiology. An initial tissue damage is responsible for an inflammatory reaction which modulates and controls tissue repair with accumulation of mesenchymal cells, an accumulation which results from their migration and replication under the influence of chemotactic and/or mitogenic mediators (cytokines). Fibrosis occurs as an accentuation of this physiological process and may be understood as a healing process that has succeeded beyond normal expectation. Studies of idiopathic pulmonary fibrosis have improved our understanding of the physiopathology of pulmonary fibrosis. Alveolitis sets in response to an initial injury of undetermined nature, and from then on lymphocytes, neutrophils and macrophages intervene in the pathological process: (1) lymphocytes contribute to the perpetuation of the process by local production of immune complexes and coactivation of other inflammatory cells; (2) neutrophils and, to a lesser extent, eosinophils worsen the initial tissue injury by producing proteases and oxydants; (3) finally, macrophages control the local accumulation of mesenchymal cells by producing chemotactic and growth factors and by modulating the secretion by these cells of extracellular matrix.
authors.affiliation: Service de pneumologie, CHRU de Nancy et INSERM Unité 14.
authors.forename: P
authors.initials: P
authors.lastname: Vaillant
authors.forename: Y
authors.initials: Y
authors.lastname: Martinet
mesh_terms: D016207:Cytokines / Q000502:physiology; D006801:Humans; D008214:Lymphocytes / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D009504:Neutrophils / Q000502:physiology; D011658:Pulmonary Fibrosis / Q000473:pathology* / Q000503:physiopathology
chemical_list: D016207:Cytokines
vernacular_title: Biopathologie des alvéolites fibrosantes.