High Blood Eosinophil Count at Stable State is Not Associated with Airway Microbiota Distinct Profile in COPD - Université de Reims Champagne-Ardenne
Article Dans Une Revue International Journal of Chronic Obstructive Pulmonary Disease Année : 2024

High Blood Eosinophil Count at Stable State is Not Associated with Airway Microbiota Distinct Profile in COPD

Résumé

Purpose: The heterogeneity of clinical features in COPD at stable state has been associated with airway microbiota. Blood eosinophil count (BEC) represents a biomarker for a pejorative evolution of COPD, including exacerbations and accelerated FEV1 decline. We aimed to analyse the associations between BEC and airway microbiota in COPD at stable state. Patients and methods: Adult COPD patients at stable state (RINNOPARI cohort) were included and characterised for clinical, functional, biological and morphological features. BEC at inclusion defined 2 groups of patients with low BEC <300/mm3 and high BEC ≥300/mm3. Sputa were collected and an extended microbiological culture was performed for the identification of viable airway microbiota. Results: Fifty-nine subjects were included. When compared with the low BEC (n=40, 67.8%), the high BEC group (n=19, 32.2%) had more frequent exacerbations (p<0.001) and more pronounced cough and sputum (p<0.05). The global composition, the number of bacteria per sample and the α-diversity of the microbiota did not differ between groups, as well as the predominant phyla (Firmicutes), or the gender repartition. Conclusion: In our study, high BEC in COPD at stable state was associated with a clinical phenotype including frequent exacerbation, but no distinct profile of viable airway microbiota compared with low BEC.
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Dates et versions

hal-04530339 , version 1 (03-04-2024)

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Jeanne-Marie Perotin, Anaëlle Muggeo, Quentin Lecomte-Thenot, Audrey Brisebarre, Sandra Dury, et al.. High Blood Eosinophil Count at Stable State is Not Associated with Airway Microbiota Distinct Profile in COPD. International Journal of Chronic Obstructive Pulmonary Disease, 2024, Volume 19, pp.765-771. ⟨10.2147/COPD.S453526⟩. ⟨hal-04530339⟩

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