Pulmonary inflammation in patients with chronic obstructive pulmonary disease with higher blood eosinophil counts

Kolsum, Umme; Damera, Gautam; Pham, Tuyet‐Hang; Southworth, Thomas; Mason, Sarah; Karur, Pradeep; Newbold, Paul; Singh, Dave

doi:10.1016/j.jaci.2017.04.027

Cited by 85 publications

(110 citation statements)

References 17 publications

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“…COPD patients were further analyzed according to current smoking and blood eosinophil counts (using a threshold of 300 cells/µL, which identifies patients with higher corticosteroid response clinically). 17 The majority of patients were ICS users (n=26 out of 32), so subanalysis based on ICS use could not be performed. For smoking status (14 current smokers versus 18 ex-smokers) and eosinophil counts (n=12 .300 cells/µL versus n=20 ,300 cells/µL), there were no significant differences between groups for drug effects ( Figures S2 and S3).…”

Section: Pbmcsmentioning

confidence: 99%

Differential anti-inflammatory effects of budesonide and a p38 MAPK inhibitor AZD7624 on COPD pulmonary cells

Higham¹,

Karur²,

Jackson³

et al. 2018

Airway Pharmacology and Treatment

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Background: The effects of anti-inflammatory drugs in COPD patients may vary between different cell types. The aim of the current study was to assess the anti-inflammatory effects of the corticosteroid budesonide and a p38 MAPK inhibitor (AZD7624) on different cell types obtained from COPD patients and healthy controls. Methods: Eight healthy smokers, 16 COPD infrequent exacerbators, and 16 frequent COPD exacerbators ($2 exacerbations in the last year) were recruited for bronchoscopy and blood sampling. The anti-inflammatory effects of budesonide and AZD7624 were assessed on cytokine release from lipopolysaccharide-stimulated alveolar macrophages and peripheral blood mononuclear cells and polyinosinic:polycytidylic acid-stimulated bronchial epithelial cells. Results: The anti-inflammatory effects of budesonide varied greatly within a patient according to the cell type studied. Bronchial epithelial cells showed the lowest sensitivity to budesonide, while peripheral blood mononuclear cells showed the greatest sensitivity. AZD7624 had a greater effect than budesonide on cytokine production from bronchial epithelial cells. Exacerbation frequency did not influence corticosteroid sensitivity. Conclusion: We observed variable corticosteroid and p38 MAPK inhibitor anti-inflammatory responses within the same individual depending on the cell type studied. These findings support the use of multiple anti-inflammatory strategies in COPD patients due to differences between cell types.

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Section: Pbmcsmentioning

confidence: 99%

Differential anti-inflammatory effects of budesonide and a p38 MAPK inhibitor AZD7624 on COPD pulmonary cells

Higham¹,

Karur²,

Jackson³

et al. 2018

Airway Pharmacology and Treatment

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“…The evidence for increased lung eosinophil numbers during the stable state and exacerbations in a subset of COPD patients suggests that these individuals might benefit from targeted pharmacological treatment directed towards eosinophils themselves and/or towards associated inflammation present in these individuals. As there is a relationship between blood and lung eosinophil counts (14,(26)(27)(28)(29)(30), it appears that BEC have potential to act as a biomarker for eosinophil-associated inflammation in the lungs.…”

Section: Introductionmentioning

confidence: 99%

Blood Eosinophil Counts in Clinical Trials for Chronic Obstructive Pulmonary Disease

Singh

Bafadhel

Brightling

et al. 2020

Am J Respir Crit Care Med

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“…Kolsum U et al reported that compared with COPD with blood EOS < 150 cells/μL, EOS% in induced sputum, BALF, and submucosa were all signi cantly increased in COPD with blood EOS > 300 cells/μL [38]. Nevertheless, several studies found that the correlation between lung tissue and blood EOS was not very well [36,39].…”

Section: Discussionmentioning

confidence: 99%

“…Many studied showed that blood EOS was considered to be a reasonably good predictor of EOS in airways in COPD patients [22,37,38]. Eltboli O et al showed that the strong correlations between blood EOS% and the submucosal eosinophil counts (r = 0.57) and reticular basement membrane (RBM) thickness (r = 0.59) were found in COPD [37].…”

Section: Discussionmentioning

confidence: 99%

Clinical differences between eosinophilic and non-eosinophilic acute exacerbation of chronic obstructive pulmonary disease (AECOPD), a multicenter cross-sectional study

Dai

Ran

Wang

et al. 2020

Preprint

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Background AECOPD is highly heterogeneous with respect to etiology and inflammation. COPD with higher blood eosinophils is associated with increased readmission rates and better corticosteroid response. However, the clinical features of eosinophilic AECOPD aren’t well explored. Then, the aim of this study was to investigate the clinical differences between eosinophilic and non-eosinophilic AECOPD. Methods A total of 643 AECOPD patients were enrolled in this multicenter cross-sectional study. Finally, 455 were included, 214 in normal eosinophils AECOPD (NEOS-AECOPD) group, 63 in mild increased eosinophils AECOPD (MEOS-AECOPD) group, and 138 in severe increased eosinophils AECOPD (SEOS-AECOPD) group. Then, demographic data, underlying diseases, symptoms, and laboratory findings were collected. Multiple logistic regression was performed to identify the independent factors associated with blood EOS. Correlations between blood EOS and its associated independent factors were evaluated. Results The significant differences in 19 factors, including underlying disease, clinical symptom, and laboratory parameters, were identified by univariate analysis. Subsequently, multiple logistic regression revealed that lymphocytes%, neutrophils% (NS%), procalcitonin (PCT), and anion gap (AG) were associated with blood EOS in AECOPD. Both blood EOS counts and EOS% significantly correlated with lymphocytes%, NS%, PCT, and AG. Conclusions The blood EOS was independently associated with lymphocytes%, NS%, PCT, and AG in AECOPD patients. Lymphocytes% was lower, and, NS%, PCT, and AG were higher in eosinophilic AECOPD. Our results indicate that viral dominant infections probably were the major etiology of eosinophilic AECOPD. Non-eosinophilic AECOPD was more likely associated with bacterial dominant infections. The systemic inflammation in non-eosinophilic AECOPD was more severe.

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Pulmonary inflammation in patients with chronic obstructive pulmonary disease with higher blood eosinophil counts

Cited by 85 publications

References 17 publications

Differential anti-inflammatory effects of budesonide and a p38 MAPK inhibitor AZD7624 on COPD pulmonary cells

Differential anti-inflammatory effects of budesonide and a p38 MAPK inhibitor AZD7624 on COPD pulmonary cells

Blood Eosinophil Counts in Clinical Trials for Chronic Obstructive Pulmonary Disease

Clinical differences between eosinophilic and non-eosinophilic acute exacerbation of chronic obstructive pulmonary disease (AECOPD), a multicenter cross-sectional study

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