Chronic Obstructive Pulmonary Disease With Eosinophilia, an Emerging Phenotype?

Villar, Adolfo Baloira; Sanmartín, Abel Pallarés

doi:10.1016/j.arbr.2016.02.012

Cited by 5 publications

(2 citation statements)

References 11 publications

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“…68 Eosinophilic COPD is related to relatively mild alveolar damage. 69 The influx and activation of eosinophils in the lungs in COPD is seen in some patients with chronic bronchitis, rather than emphysema. However, whether this eosinophilia is independent of asthmatic etiology during COPD progression is still controversial.…”

Section: Eosinophilsmentioning

confidence: 99%

<p>How Do Innate Immune Cells Contribute to Airway Remodeling in COPD Progression?</p>

Bu¹,

Wang²,

Yin³

2020

COPD

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Recently, the therapeutic potential of immune-modulation during the progression of chronic obstructive pulmonary disease (COPD) has been attracting increasing interest. However, chronic inflammatory response has been oversimplified in descriptions of the mechanism of COPD progression. As a form of first-line airway defense, epithelial cells exhibit phenotypic alteration, and participate in epithelial layer disorganization, mucus hypersecretion, and extracellular matrix deposition. Dendritic cells (DCs) exhibit attenuated antigen-presenting capacity in patients with advanced COPD. Immature DCs migrate into small airways, where they promote a pro-inflammatory microenvironment and bacterial colonization. In response to damageassociated molecular patterns (DAMPs) in lung tissue affected by COPD, neutrophils are excessively recruited and activated, where they promote a proteolytic microenvironment and fibrotic repair in small airways. Macrophages exhibit decreased phagocytosis in the large airways, while they demonstrate high pro-inflammatory potential in the small airways, and mediate alveolar destruction and chronic airway inflammation. Natural killer T (NKT) cells, eosinophils, and mast cells also play supplementary roles in COPD progression; however, their cellular activities are not yet entirely clear. Overall, during COPD progression, "exhausted" innate immune responses can be observed in the large airways. On the other hand, the innate immune response is enhanced in the small airways. Approaches that inhibit the inflammatory cascade, chemotaxis, or the activation of inflammatory cells could possibly delay the progression of airway remodeling in COPD, and may thus have potential clinical significance.

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Section: Eosinophilsmentioning

confidence: 99%

<p>How Do Innate Immune Cells Contribute to Airway Remodeling in COPD Progression?</p>

Bu¹,

Wang²,

Yin³

2020

COPD

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“…Emerging evidence shows a potential role for eosinophilic inflammation indicating distinctive clinical features in COPD and a potential marker for tailored treatment approach. 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 Our aim in this study was to evaluate eosinophilic inflammation and its' relation to the clinical characteristics of COPD patients such as exacerbation history, LTOT, and domiciliary noninvasive mechanical ventilation (NIMV).…”

Section: Introductionmentioning

confidence: 99%

Long‐term oxygen treatment need is less frequent in eosinophilic COPD patients

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Aydın-Güçlü

et al. 2021

Clinical Respiratory J

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Introduction Eosinophilic airway inflammation is a recognized inflammatory pattern in subgroups of patients with chronic obstructive pulmonary disease (COPD). However, there are still conflicting results between various studies concerning the effect of eosinophils in COPD patients. Our aim with this study was to evaluate eosinophilic inflammation and its relation to the clinical characteristics in a group of COPD patients. Methods Stable COPD patients with FEV1% predicted < 50 or with ≥ 1 exacerbation leading to hospital admission or ≥2 moderate or severe exacerbation history were consecutively enrolled from outpatient clinics. Results We included 90 male COPD patients, with a mean age of 63.3 ± 9.2. Mean FEV1% predicted was 35.9 ± 11.3. Eosinophilic inflammation (eosinophil percentage ≥2%) was evident in 54 (60%) of the patients. Participants with eosinophilic inflammation were significantly older and had better FEV1 predicted % values. Eosinophilic COPD patients were characterized with better quality of life and fewer symptoms. COPD patients with noneosinophilic inflammation used supplemental long‐term oxygen therapy (LTOT) more frequently compared to patients with eosinophilic inflammation (36.1% vs. 14.8%, p = 0.01). Eosinophilic inflammation is associated with less dyspnea severity measured by mMRC (OR: 0.542 95% CI: 0.342–0.859, p = 0.009) and less LTOT use (OR: 0.334 95% CI: 0.115–0.968, p = 0.04) regardless of age, severity of airflow limitation, and having frequent exacerbation phenotype. Conclusion Our study supports the growing evidence for a potential role of eosinophilic inflammation phenotype in COPD with distinctive clinical characteristics. Eosinophilic inflammation is inversely associated with dyspnea severity measured by mMRC and LTOT use independently from age, total number of exacerbations, St. George Respiratory Questionnaire (SGRQ) total score and FEV1% predicted.

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