title: Contribution of bronchial biopsies in the evaluation of pathogenesis and progression of COPD.
abstract: This review summarizes and discusses the lung pathology of COPD patients emphasising on inflammatory cell phenotypes and mechanisms which prevail in different clinical conditions. In bronchial biopsies a series of events takes place during the progression of the disease from mild to severe. T-lymphocytes, particularly CD8+ cells and macrophages are the prevalent inflammatory cells in the lungs of healthy smokers and patients with mild/moderate COPD. This T-cell activation seems to be sustained by CD4+, CD8+ cells and macrophages expressing transcription factors and Tc1 cytokines such as NF-kB, STAT4 and IFNgamma. In contrast, severe disease is characterized by lymphocytes producing greater amounts of TGF-beta1 and by an increase of nitrotyrosine immunoreactivity and activated neutrophils, macrophages and MPO+ cells. However, the mechanisms involved in neutrophilic migration and adhesion are currently under investigation. Recent data has shown that in severe COPD there is an impaired neutrophil capability to respond to chemotactic stimuli, as well as an increased collagen adhesion of neutrophils due to the up-regulation of CD44 and CD11b receptors. This data together, may account for the increased neutrophilia observed in the severe disease states of COPD. In this context, insights obtained from the tissutal analysis of bronchial biopsies represent an irreplaceable route to further progresses in to the pathogenesis of this disease.
authors.affiliation: Università degli Studi di Palermo, Dipartimento di Medicina Sperimentale, Sezione Anatomia Umana, Via del Vespro 129, 90127 Palermo, Italy. francymagno@libero.it
authors.forename: F
authors.initials: F
authors.lastname: Magno
authors.forename: A
authors.initials: A
authors.lastname: Di Stefano
mesh_terms: D001706:Biopsy; D001980:Bronchi / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*