RATIONALE: 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. OBJECTIVES: 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. MEASUREMENTS AND MAIN 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.
RATIONALE: 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. OBJECTIVES: 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. MEASUREMENTS AND MAIN 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: Francesca Polverino; Borja G Cosio; Jaime Pons; Maria Laucho-Contreras; Paula Tejera; Amanda Iglesias; Angel Rios; Andreas Jahn; Jaume Sauleda; Miguel Divo; Victor Pinto-Plata; Lynette Sholl; Ivan O Rosas; Alvar Agustí; Bartolome R Celli; Caroline A Owen Journal: Am J Respir Crit Care Med Date: 2015-09-15 Impact factor: 21.405
Authors: Amit A Lugade; R Robert Vethanayagam; Mehrab Nasirikenari; Paul N Bogner; Brahm H Segal; Yasmin Thanavala Journal: Am J Respir Cell Mol Biol Date: 2011-01-07 Impact factor: 6.914
Authors: Francesca Polverino; Melanie Doyle-Eisele; Jacob McDonald; Julie A Wilder; Christopher Royer; Maria Laucho-Contreras; Emer M Kelly; Miguel Divo; Victor Pinto-Plata; Joe Mauderly; Bartolome R Celli; Yohannes Tesfaigzi; Caroline A Owen Journal: Am J Pathol Date: 2014-12-24 Impact factor: 4.307
Authors: Francesca Polverino; Leen J M Seys; Ken R Bracke; Caroline A Owen Journal: Am J Physiol Lung Cell Mol Physiol Date: 2016-08-19 Impact factor: 5.464
Authors: Tsung-Chieh Yao; Gaixin Du; Lide Han; Ying Sun; Donglei Hu; James J Yang; Rasika Mathias; Lindsey A Roth; Nicholas Rafaels; Emma E Thompson; Dagan A Loisel; Rebecca Anderson; Celeste Eng; Maitane Arruabarrena Orbegozo; Melody Young; James M Klocksieben; Elizabeth Anderson; Kathleen Shanovich; Lucille A Lester; L Keoki Williams; Kathleen C Barnes; Esteban G Burchard; Dan L Nicolae; Mark Abney; Carole Ober Journal: J Allergy Clin Immunol Date: 2013-08-06 Impact factor: 10.793