Three-year follow-up of Interleukin 6 and C-reactive protein in chronic obstructive pulmonary disease

Ferrari, Renata; Tanni, Suzana Erico; Caram, Laura; Corrêa, Corina; Corrêa, Camila Renata; Godoy, Irma

doi:10.1186/1465-9921-14-24

Cited by 73 publications

(65 citation statements)

References 31 publications

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“…• ■ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ▲ ■ reported that IL-6 concentration is increased in the peripheral blood of COPD patients, and represents a reliable marker of systemic inflammation discriminating between COPD patients and smokers without COPD [40,41]. Our data indicate that IL-6 mediates the priming effect of the COPD bronchial epithelium on B-cells for IgA synthesis.…”

Section: Both Maturation Of B-cells Into Cd38mentioning

confidence: 99%

Increased IgA production by B-cells in COPDvialung epithelial interleukin-6 and TACI pathways

et al. 2014

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Despite their relevance to mucosal defense, production of IgA and the function of lung B-cells remain unknown in chronic obstructive pulmonary disease (COPD).We assessed IgA synthesis in the lungs of COPD (n=28) and control (n=21) patients, and regulation of B-cells co-cultured with in vitro-reconstituted airway epithelium.In COPD lung tissue, synthesis of IgA1 was increased, which led to its accumulation in subepithelial areas. In vitro, the COPD bronchial epithelium imprinted normal human B-cells for increased production of IgA (mainly IgA1) and maturation into CD38 + plasma cells. These effects were associated with upregulation of TACI (transmembrane activator and CAML interactor) and were observed under resting conditions, while being partly inhibited upon stimulation with cigarette smoke extract. Interleukin (IL)-6 and BAFF (B-cell activating factor)/APRIL (a proliferation-inducing ligand) were upregulated in the COPD epithelium and lung tissue, respectively; the IgA-promoting effect of the COPD bronchial epithelium was inhibited by targeting IL-6 and, to a lower extent, by blocking TACI.These data show that in COPD, the bronchial epithelium imprints B-cells with signals promoting maturation into IgA-producing plasma cells through the action of two epithelial/B-cell axes, namely the IL-6/IL-6 receptor and BAFF-APRIL/TACI pathways, while cigarette smoke partly counteracts this IgApromoting effect. @ERSpublications COPD epithelium induces B-cell maturation of IgA-producing plasma cells via IL-6/IL-6R and BAFF-APRIL/TACI pathways

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Section: Both Maturation Of B-cells Into Cd38mentioning

confidence: 99%

Increased IgA production by B-cells in COPDvialung epithelial interleukin-6 and TACI pathways

et al. 2014

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“…These include more frequent exacerbations, greater risk of co-morbid disease (pneumonia, lung cancer, coronary artery disease and heart failure) and greater mortality [8, [84][85][86][87]. We suggest that it is time to urgently examine the potential utility of existing 'cardioprotective therapies' in patients with COPD (± systemic inflammation) to test their effects on morbidity and mortality.…”

Section: Figure 6 Statin Use and Chest Infections (Pneumonia And Infmentioning

confidence: 97%

“…disease, greater tendency to infective exacerbations and greater mortality from pneumonia and lung cancer [8, [84][85][86][87]. To date, treatment of COPD has been limited to inhaler-based therapy aimed at minimizing symptoms due to airway inflammation and bronchoconstriction.…”

Section: Expert Commentarymentioning

confidence: 99%

Update on the potential role of statins in chronic obstructive pulmonary disease and its co-morbidities

Young¹,

Hopkins

2013

Expert Review of Respiratory Medicine

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Chronic obstructive pulmonary disease (COPD) is soon to become the third leading cause of death in developed countries. COPD is increasingly considered a multisystem disease characterized by both pulmonary and systemic inflammation. Over the last 5 years, there have been a growing number of studies showing that the cholesterol-lowering drugs statins (HMG-CoA reductase inhibitors) have a beneficial effect in patients with COPD. While statins are known to have a number of pharmacological effects (pleiotropy) that could explain these benefits, it is currently not clear which effects are most relevant in COPD. This article reviews the most recently published studies of statin therapy in patients with COPD, focusing on the important COPD co-morbidities of the pulmonary system (infective exacerbations, pneumonia, influenza and lung cancer) and cardiovascular system (acute coronary syndrome, endothelial dysfunction and pulmonary hypertension). While we await the results of randomized controlled trials, there continues to be consistent (albeit indirect) evidence from observational studies suggesting statins are beneficial for patients with COPD, conferring important pharmacological effects on inflammation not conferred by current inhaler-based therapies.

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“…It is secreted by a variety of lymphoid and non-lymphoid cells including T cells, B cells, monocytes, fibroblasts, hepatocytes, airway endothelial cells, alveolar macrophages, adipocytes, and myocytes as well as other tissues and cells (Hayashi et al, 2000;Fredj et al, 2005;He et al, 2009;Sofi et al, 2009). Accumulated evidence has suggested that IL-6 is involved in the development of COPD (Ferrari et al, 2013), with many clinical studies having reported that IL-6 polymorphisms affect the susceptibility of patients to COPD (Seifart et al, 2005;Broekhuizen et al, 2005;Córdoba-Lanús et al, 2008;He et al, 2009;Yanbaeva et al, 2006Yanbaeva et al, , 2009. One such polymorphism is the IL-6-174G>C (also called rs1800795) polymorphism in the IL-6 promoter.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-6 gene -174G>C polymorphism and chronic obstructive pulmonary disease risk: a meta-analysis

Xie¹,

Ke²,

Yh³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Association studies of interleukin-6 (IL-6) -174G>C polymorphism and chronic obstructive pulmonary disease (COPD) have yielded inconsistent results, possibly because single studies often lack sufficient statistical power. A comprehensive search was performed in the PubMed, Embase, Elsevier, Web of Science databases, Wanfang, and the Chinese National Knowledge Infrastructure (CNKI) databases for published studies investigating the associations between IL-6 -174G>C polymorphism and COPD. Odds ratios (OR) and 95% confidence intervals (95%CI) were used to assess the possible associations. Seven studies with a total of 2701 subjects were included in this meta-analysis. A significantly increased risk was detected in the C allele of the IL-6 -174G>C in Caucasians (C vs G: OR = 1.16, 95%CI = 1.03-1.30; CC+GC vs GG: OR = 1.21, 95%CI = 1.02-1.42; CC vs GG: OR = 1.32, 95%CI = 1.03-1.70). This meta-analysis suggests that the C allele of the IL-6 -174G>C might act as a COPD risk factor in 8517 IL-6 polymorphism and COPD risk ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 8516-8525 (2015) Caucasians. Further well-designed case-control studies with larger sample sizes are needed to confirm these conclusions.

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Three-year follow-up of Interleukin 6 and C-reactive protein in chronic obstructive pulmonary disease

Cited by 73 publications

References 31 publications

Increased IgA production by B-cells in COPDvialung epithelial interleukin-6 and TACI pathways

Increased IgA production by B-cells in COPDvialung epithelial interleukin-6 and TACI pathways

Update on the potential role of statins in chronic obstructive pulmonary disease and its co-morbidities

Interleukin-6 gene -174G>C polymorphism and chronic obstructive pulmonary disease risk: a meta-analysis

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