title: A novel insight into adaptive immunity in chronic obstructive pulmonary disease: B cell activating factor belonging to the tumor necrosis factor family.
abstract: BACKGROUND
  Chronic obstructive pulmonary disease (COPD) is a disorder characterized by an abnormal inflammatory response that persists even after smoking cessation, yet the underlying mechanisms are not fully understood.
  
  
  OBJECTIVE
  To investigate the expression of B-cell activating factor of tumor necrosis factor family (BAFF), a crucial mediator in the crosstalk between innate and adaptive immune responses, in patients with COPD and to explore its correlation with disease severity.
  
  
  METHODS
  Using immunohistochemistry, expression of BAFF was examined in lung specimens from 21 smokers with COPD (FEV(1) = 57 ± 5% predicted), 14 control smokers (FEV(1) = 99 ± 2% predicted) and 8 nonsmokers (FEV(1) = 104 ± 4% predicted). BAFF was quantified in alveolar macrophages and alveolar walls, in bronchiolar and parenchymal lymphoid follicles, and in peripheral airways and pulmonary arterioles.
  
  
  RESULTS
  In alveolar macrophages and parenchymal lymphoid follicles, BAFF expression was increased in smokers with COPD compared with control smokers and nonsmokers (P < 0.05 for all comparisons). In both compartments, BAFF was also up-regulated in control smokers as compared with nonsmokers (P = 0.03 and P = 0.01). Moreover, BAFF was overexpressed in bronchiolar lymphoid follicles, alveolar walls, peripheral airways, and pulmonary arterioles from smokers with COPD compared with nonsmokers (P < 0.05 for all). Among patients with COPD, BAFF(+) macrophages were inversely related to FEV(1) (P = 0.03, Spearman's rho [r(S)] = -0.48), FEV(1)/FVC (P = 0.02, r(S) = -0.50), and Pa(O(2)) values (P = 0.01, r(S) = -0.55).
  
  
  CONCLUSIONS
  This study demonstrated overexpression of BAFF in peripheral lung of patients with COPD, mainly in alveolar macrophages and lymphoid follicles. Moreover, BAFF expression was correlated to the degree of lung function impairment and hypoxia, suggesting that it may have a possible impact on disease severity.
authors.affiliation: Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova and Padova City Hospital, 35128 Padova, Italy.
authors.forename: Francesca
authors.initials: F
authors.lastname: Polverino
authors.forename: Simonetta
authors.initials: S
authors.lastname: Baraldo
authors.forename: Erica
authors.initials: E
authors.lastname: Bazzan
authors.forename: Simone
authors.initials: S
authors.lastname: Agostini
authors.forename: Graziella
authors.initials: G
authors.lastname: Turato
authors.forename: Francesca
authors.initials: F
authors.lastname: Lunardi
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Balestro
authors.forename: Marco
authors.initials: M
authors.lastname: Damin
authors.forename: Alberto
authors.initials: A
authors.lastname: Papi
authors.forename: Piero
authors.initials: P
authors.lastname: Maestrelli
authors.forename: Fiorella
authors.initials: F
authors.lastname: Calabrese
authors.forename: Marina
authors.initials: M
authors.lastname: Saetta
mesh_terms: D056704:Adaptive Immunity; D053264:B-Cell Activating Factor / Q000378:metabolism*; D053265:B-Cell Activation Factor Receptor / Q000378:metabolism; D015415:Biomarkers; D016022:Case-Control Studies; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007150:Immunohistochemistry; D008168:Lung / Q000276:immunology / Q000473:pathology; D016131:Lymphocyte Subsets / Q000378:metabolism; D008221:Lymphoid Tissue / Q000276:immunology; D016676:Macrophages, Alveolar / Q000276:immunology; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D012720:Severity of Illness Index; D016037:Single-Blind Method; D012907:Smoking / Q000009:adverse effects / Q000276:immunology*
chemical_list: D053264:B-Cell Activating Factor; D053265:B-Cell Activation Factor Receptor; D015415:Biomarkers