Multiple Circulating Cytokines Are Coelevated in Chronic Obstructive Pulmonary Disease

Selvarajah, Senthooran; Todd, Ian; Tighe, Patrick J.; John, Michelle; Bolton, Charlotte E.; Harrison, Timothy; Fairclough, Lucy

doi:10.1155/2016/3604842

Cited by 30 publications

(18 citation statements)

References 33 publications

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“…Furthermore, it was revealed that in the COPD patients with various cardiovascular diseases, the number of non-emphysema patients was greater than the number of emphysema patients; however, there was no statistically significant difference among the different severities of emphysema. Previous studies on COPD patients with atrial fibrillation demonstrated that recurrent episodes of systemic and local chronic airway inflammation, as well as continuous increases of inflammatory mediators in the circulating blood, are important factors leading to arteriosclerosis and increased cardiovascular events caused by the dysfunction of vascular endothelium (26)(27)(28). In the present study, the levels of MMP-9 in COPD patients with cardiovascular disease were higher than those in patients without cardiovascular disease.…”

Section: Discussionsupporting

confidence: 41%

Effect of the emphysema subtypes of patients with chronic obstructive pulmonary disease on airway inflammation and COTE index

et al. 2018

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The aim of the present study was investigate the association of the severity of emphysema of patients with chronic obstructive pulmonary disease (COPD) with airway inflammation and the COPD-specific comorbidity test (COTE) index. A total of 94 patients with COPD were divided into four groups according to the severity of their emphysema; in each patient, comorbidities were recorded and inflammatory biomarkers, including MMP-9 and TIMP-1 were determined in circulating blood. The unbalanced proportion of MMP-9 and its inhibitor, TIMP-1, led to the airway inflammation and lung remodeling in the patients with COPD. A total of 80.85% of the patients had emphysema of different degrees. The quantity of male patients and the smoking index in the three emphysema groups were significantly higher than those in the non-emphysema group (F=7.67 and 5.42, P<0.05). The level of the predicted percent offorced expiratory volume in 1 sec in the non-emphysema group were significantly higher than those in the emphysema group (4.33; P<0.05), and the level of D-dimer in the non-emphysema group was significantly lower than that in the mild and moderate emphysema groups (F=9.38, P<0.05). The low-attenuation area score was negatively correlated with inhaled bronchodilators (r=-0.240, P= 0.007) but positively correlated with the frequency of acute exacerbations in the previous year (r=0.211, P=0.001). In terms of treatment, the use of systemic hormone therapy in the emphysema group was more frequent than that in the non-emphysema group (F=6.21, 12.92 and 4.08, P<0.05). The level of MMP-9 was significantly higher in COPD patients with >3 comorbidities, a COTE index of ≥4 and cardiovascular disease as well as coronary heart disease (t=6.40, 2.53, 3.65 and 2.90, P<0.05). The level of MMP-9 was positively correlated with the neutrophilic granulocyte percentage, the number of comorbidities and the COTE index (r=0.193, 0.402 and 0.311, P<0.01). The severity of emphysema in patients with COPD was correlated with the persistence of inflammatory factors in the circulating blood and the frequency of acute exacerbations. It was indicated that MMP-9 has a critical role in numerous comorbidities of COPD.

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Section: Discussionsupporting

confidence: 41%

Effect of the emphysema subtypes of patients with chronic obstructive pulmonary disease on airway inflammation and COTE index

et al. 2018

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“…Overall, cytokine concentration differences between groups were not statistically significant. However, the researchers uncovered that the total serum cytokine levels statistically correlated with GOLD-determined COPD severity [ 67 ]. Given the assay sensitivity and serum access, this may be a fruitful way to identify patient risks prior to phenotypic symptoms and exacerbations.…”

Section: Introductionmentioning

confidence: 99%

Precision medicine in COPD: where are we and where do we need to go?

2018

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Chronic obstructive pulmonary disease (COPD) was the fourth leading cause of death worldwide in 2015. Current treatments for patients ease discomfort and help decrease disease progression; however, none improve lung function or change mortality. COPD is heterogeneous in its molecular and clinical presentation, making it difficult to understand disease aetiology and define robust therapeutic strategies. Given the complexity of the disease we propose a precision medicine approach to understanding and better treating COPD. It is possible that multiOMICs can be used as a tool to integrate data from multiple fields. Moreover, analysis of electronic medical records could aid in the treatment of patients and in the predictions of outcomes. The Precision Medicine Initiative created in 2015 has made precision medicine approaches to treat disease a reality; one of these diseases being COPD.

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“…Multiple studies (21)(22)(23)(24) reported that patients with cardiovascular disease, diabetes, depression, cancer, and other diseases can show accelerated progression of COPD, and that an increase of C-reactive protein, interleukin-6, interleukin-8, and other markers can also accelerate the process of COPD. The results of this study indicated that in COPD patients with more than three comorbidities, the status of the smoking group was not more severe than that of the nonsmoking group, and that according to CT types, the status of type M patients with more than three comorbidities was more severe than that of type A patients.…”

Section: Discussionmentioning

confidence: 99%

“…There were no differences among the subgroups in the nonsmoking group, indicating that the inflammatory mediators produced by harmful substances in the smoke also aggravate the development of comorbidities in the circulation. Other studies (24,25) showed that in COPD patients with moderate and severe cardiovascular and metabolic diseases, a variety of inflammatory mediators exist in circulating blood. In the type M and type E smoking groups, the status of COPD patients with cardiovascular disease was more serious than that of type A patients; in the nonsmoking group, there were no differences among the three subtypes in COPD patients with cardiovascular disease, indicating that although patients had quit smoking, chronic inflammatory mediators persisted in the blood of those with COPD and cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Typing of chronic obstructive pulmonary disease using high-resolution computed tomography and the association with smoking, airway inflammation, and common comorbidities

Liu¹,

Wang²,

Liu³

et al. 2018

Turk J Med Sci

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Background/aim: This study performed typing of chronic obstructive pulmonary disease (COPD) using high-resolution computed tomography (HRCT) to determine the association with smoking, matrix metalloproteinases, and common comorbidities. Materials and methods:The study enrolled 94 hospitalized patients. Participants were divided into a group of 69 current and former smokers (group A) and a group of 25 that had never smoked (group B). Patients were also divided into 3 categories according to the degree of emphysema and bronchial wall thickness using HRCT to determine the association with levels of matrix metalloproteinase 9 (MMP-9) and TIMP-1, as well as associated comorbidities. These three categories were: type A -no or mild emphysema, with or without bronchial wall thickening; type E -emphysema without bronchial wall thickening; and type M -both emphysema and bronchial wall thickening. Results:The low attenuation area (LAA) scores in group A patients were higher than those in group B (t = 2.86, P < 0.01); correlation analysis showed that smoking was associated with a decline of the forced expiratory volume in 1 s and forced vital capacity ratio (FEV1/ FVC%) and higher LAA scores in patients with COPD (F = 4.46, F = 8.20, P < 0.05). The levels of MMP-9 in group A were higher than those in group B (t = 3.65, P < 0.01). Among COPD patients with more than 3 comorbidities, there were statistically significant differences in both the smoking group and the nonsmoking group (chi-square = 12.08, P < 0.01). When compared to type A patients, who had coincident cardiovascular diseases in the smoking group, patients of type M and E showed statistically significant differences (F = 2.42 and 2.12, P < 0.05). Conclusion:Emphysema was more severe in smokers. Metalloproteinase levels in smokers were higher than those in nonsmokers. Moreover, comorbidities were more severe in smokers.

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Multiple Circulating Cytokines Are Coelevated in Chronic Obstructive Pulmonary Disease

Cited by 30 publications

References 33 publications

Effect of the emphysema subtypes of patients with chronic obstructive pulmonary disease on airway inflammation and COTE index

Effect of the emphysema subtypes of patients with chronic obstructive pulmonary disease on airway inflammation and COTE index

Precision medicine in COPD: where are we and where do we need to go?

Typing of chronic obstructive pulmonary disease using high-resolution computed tomography and the association with smoking, airway inflammation, and common comorbidities

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