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A novel insight into adaptive immunity in chronic obstructive pulmonary disease: B cell activating factor belonging to the tumor necrosis factor family.
Am J Respir Crit Care Med. 2010 Oct 15; 182(8):1011-9.AJ

Abstract

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+Show Affiliations

Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova and Padova City Hospital, 35128 Padova, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20581172

Citation

Polverino, Francesca, et al. "A Novel Insight Into Adaptive Immunity in Chronic Obstructive Pulmonary Disease: B Cell Activating Factor Belonging to the Tumor Necrosis Factor Family." American Journal of Respiratory and Critical Care Medicine, vol. 182, no. 8, 2010, pp. 1011-9.
Polverino F, Baraldo S, Bazzan E, et al. A novel insight into adaptive immunity in chronic obstructive pulmonary disease: B cell activating factor belonging to the tumor necrosis factor family. Am J Respir Crit Care Med. 2010;182(8):1011-9.
Polverino, F., Baraldo, S., Bazzan, E., Agostini, S., Turato, G., Lunardi, F., Balestro, E., Damin, M., Papi, A., Maestrelli, P., Calabrese, F., & Saetta, M. (2010). A novel insight into adaptive immunity in chronic obstructive pulmonary disease: B cell activating factor belonging to the tumor necrosis factor family. American Journal of Respiratory and Critical Care Medicine, 182(8), 1011-9. https://doi.org/10.1164/rccm.200911-1700OC
Polverino F, et al. A Novel Insight Into Adaptive Immunity in Chronic Obstructive Pulmonary Disease: B Cell Activating Factor Belonging to the Tumor Necrosis Factor Family. Am J Respir Crit Care Med. 2010 Oct 15;182(8):1011-9. PubMed PMID: 20581172.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A novel insight into adaptive immunity in chronic obstructive pulmonary disease: B cell activating factor belonging to the tumor necrosis factor family. AU - Polverino,Francesca, AU - Baraldo,Simonetta, AU - Bazzan,Erica, AU - Agostini,Simone, AU - Turato,Graziella, AU - Lunardi,Francesca, AU - Balestro,Elisabetta, AU - Damin,Marco, AU - Papi,Alberto, AU - Maestrelli,Piero, AU - Calabrese,Fiorella, AU - Saetta,Marina, Y1 - 2010/06/25/ PY - 2010/6/29/entrez PY - 2010/6/29/pubmed PY - 2010/11/16/medline SP - 1011 EP - 9 JF - American journal of respiratory and critical care medicine JO - Am J Respir Crit Care Med VL - 182 IS - 8 N2 - 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. SN - 1535-4970 UR - https://www.unboundmedicine.com/medline/citation/20581172/A_novel_insight_into_adaptive_immunity_in_chronic_obstructive_pulmonary_disease:_B_cell_activating_factor_belonging_to_the_tumor_necrosis_factor_family_ L2 - https://www.atsjournals.org/doi/10.1164/rccm.200911-1700OC?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -