Abstract
BackgroundChronic obstructive pulmonary disease (COPD) exacerbations are acute events of worsened respiratory symptoms and enhanced inflammation partly mediated by NF-κB activation. RelB, an NF-κB family member, suppresses cigarette smoke-induced inflammation but its expression in COPD is unknown. Moreover, there is no information on its association with clinical features of COPD. The objectives of this study were to assess RelB expression relative to markers of inflammation as well as its association with cardiovascular and pulmonary features of COPD patients at stable-state and exacerbation.MethodsData from 48 COPD patients were analyzed. Blood samples were collected from stable-state and exacerbating patients. After RNA isolation, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to assess RelB, Cox-2, IL-8 and IL-1β mRNA expression and their associations with measured clinical variables.ResultsOf the 48 COPD subjects, 18 were in stable-state and 30 were in exacerbation. RelB mRNA expression was lower than that of Cox-2, IL-8, and IL-1β in all cases (all p<0.001, except for IL-8 at exacerbation (p = 0.22)). Cox-2, IL-8 and IL-1β were significantly associated with clinical features of patients in both stable-state and at exacerbation. There was no association with RelB expression and any clinical features in COPD subjects at stable-state. RelB mRNA levels were significantly associated with cardiovascular events such as systolic blood pressure during exacerbation.ConclusionsRelB mRNA expression is lower than that of the other inflammatory mediators. Expression of Cox-2, IL-8 and IL-1β were related to clinical features in both stable-state and at exacerbation. However, RelB expression was associated with clinical features of patients only during exacerbation, suggesting that RelB may represent a novel marker of health outcomes, in particular cardiovascular, during exacerbation in COPD.
Highlights
Chronic obstructive pulmonary disease (COPD) is characterized by progressive, not fully reversible airflow limitation [1] and chronic inflammation [2]
nuclear factor-kB (NF-kB) is a ubiquitous transcription factor family composed of five proteins [15] activated by cigarette smoke (CS) that collectively are involved in the regulation of gene expression for pro-inflammatory cytokines, chemokines and adhesion molecules [12,16]
We have shown that loss of RelB expression due to smoke exposure promotes pro-inflammatory mediator production, whereas RelB reconstitution reduces inflammation associated with CS [23,24]
Summary
Chronic obstructive pulmonary disease (COPD) is characterized by progressive, not fully reversible airflow limitation [1] and chronic inflammation [2]. NF-kB is a ubiquitous transcription factor family composed of five proteins [15] activated by cigarette smoke (CS) that collectively are involved in the regulation of gene expression for pro-inflammatory cytokines, chemokines and adhesion molecules [12,16]. These include interleukin (IL)-1b, a key orchestrator of the immune response in COPD [14] that can activate NF-kB and is produced by airway epithelial cells in response to CS or acute injury [14,17]. Chronic obstructive pulmonary disease (COPD) exacerbations are acute events of worsened respiratory symptoms and enhanced inflammation partly mediated by NF-kB activation. The objectives of this study were to assess RelB expression relative to markers of inflammation as well as its association with cardiovascular and pulmonary features of COPD patients at stable-state and exacerbation
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