Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis

Abstract

Background: Individuals with chronic obstructive pulmonary disease (COPD) are at increased risk of cardiovascular diseases, osteoporosis, and muscle wasting. Systemic inflammation may be involved in the pathogenesis of these disorders. A study was undertaken to determine whether systemic inflammation is present in stable COPD. Methods: A systematic review was conducted of studies which reported on the relationship between COPD, forced expiratory volume in 1 second (FEV 1 ) or forced vital capacity (FVC), and levels of various systemic inflammatory markers: C-reactive protein (CRP), fibrinogen, leucocytes, tumour necrosis factor-a (TNF-a), and interleukins 6 and 8. Where possible the results were pooled together to produce a summary estimate using a random or fixed effects model. Results: Fourteen original studies were identified. Overall, the standardised mean difference in the CRP level between COPD and control subjects was 0.53 units (95% confidence interval (CI) 0.34 to 0.72). The standardised mean difference in the fibrinogen level was 0.47 units (95% CI 0.29 to 0.65). Circulating leucocytes were also higher in COPD than in control subjects (standardised mean difference 0.44 units (95% CI 0.20 to 0.67)), as were serum TNF-a levels (standardised mean difference 0.59 units (95% CI 0.29 to 0.89)). Conclusions: Reduced lung function is associated with increased levels of systemic inflammatory markers which may have important pathophysiological and therapeutic implications for subjects with stable COPD.

MicroRNA-223 controls the expression of histone deacetylase 2: a novel axis in COPD

“…IL-1β and TNFα [2,3]. As demonstrated in Figure 3B, stimulation of HPAEC with IL-1β and TNFα increased the levels of miR-223 at all time points assessed.…”

“…In stimulation experiments using endothelial cells that, in vivo, reflect the first responders of the lungs to these proinflammatory signals, we found that IL-1β and TNFα significantly induced the levels of miR-223 in a time-dependent manner. These cytokines have been described as key inflammatory mediators in COPD [2,3] and their activity in COPD patients might explain the significant upregulation of miR-223 levels in vivo as shown by Ezzie and colleagues [21]. Both cytokines are activators of the transcription factor nuclear factor kappa B (NF-κB).…”

“…Cigarette smoke and other noxious particles are important risk factors by inducing the release of inflammatory mediators such as tumor necrosis factor (TNF) α [2], interleukin 1 (IL-1) β [3] and chemokines [4]. These factors, among other mechanisms, lead to infiltration of the airway epithelium with inflammatory cells, chronic bronchial inflammation and consecutive tissue destruction [5].…”

Prevalence of chronic obstructive pulmonary disease (COPD) among rheumatoid arthritis: results from national inpatient database

“…The mechanism of COPD in RA has been suggested by prior studies to be autoimmune or inflammatory, with cytokines and chemokines contributing to lung tissue destruction [1,8,9]. Studies looking at association of reduced lung function tests with systemic inflammatory markers have shown that COPD patients have higher levels of circulating inflammatory markers including leukocytes, fibrinogen, ESR, CRP, tumor necrosis factor-α, suggesting that systemic inflammation may have a role in COPD [11]. Also, increased production of autoantibodies against a broad spectrum of self-antigens has been demonstrated in COPD, suggesting the role of autoimmunity [12].…”

Nutritional depletion and its relationship to respiratory impairment in patients with chronic respiratory failure due to COPD or restrictive thoracic diseases

“…In COPD, lung hyperinflation seems to be one factor of interest as it results in a mechanical disadvantage, although the contribution of increased work of breathing to cachexia is not clear (Engelen et al, 1999;Mannix et al, 1999;Budweiser et al, 2005Budweiser et al, , 2006b). Conversely, evidence has been accumulated that suggests a relationship to elevated levels of inflammatory cytokines and the systemic manifestation of the disease (Gan et al, 2004;Broekhuizen et al, 2006).…”