Elastin-derived peptides favor type 2 innate lymphoid cells in COPD.
Fiche publication
Date publication
mai 2024
Journal
American journal of physiology. Lung cellular and molecular physiology
Auteurs
Membres identifiés du Cancéropôle Est :
Pr LE NAOUR Richard, Dr AUDONNET Sandra , Dr POMMIER Arnaud , Dr POTTEAUX Stéphane
Tous les auteurs :
Lahire S, Fichel C, Rubaszewski O, Lereverend C, Audonnet S, Visneux V, Perotin JM, Deslée G, Le Jan S, Potteaux S, Le Naour R, Pommier A
Lien Pubmed
Résumé
Chronic obstructive pulmonary disease (COPD) is a condition characterized by chronic airway inflammation and obstruction, primarily caused by tobacco smoking. Although the involvement of immune cells in COPD pathogenesis is well established, the contribution of innate lymphoid cells (ILC) remains poorly understood. ILC are a type of innate immune cells that participate in tissue remodeling processes, but their specific role in COPD has not been fully elucidated. During COPD, the breakdown of pulmonary elastin generates elastin peptides that elicit biological activities on immune cells. This study aimed to investigate the presence of ILC in COPD patients and examine the impact of elastin peptides on their functionality. Our findings revealed an elevated proportion of ILC2 in the peripheral blood of COPD patients, and a general activation of ILC as indicated by an increase in their cytokine secretion capacity. Notably, our study demonstrated that serum from COPD patients promotes ILC2 phenotype, likely due to the elevated concentration of IL-5, a cytokine known to favor ILC2 activation. Furthermore, we uncovered that this increase in IL-5 secretion is partially attributed to its secretion by macrophages upon stimulation by elastin peptides, suggesting an indirect role of elastin peptides on ILC in COPD. These findings shed light on the involvement of ILC in COPD and provide insights into the potential interplay between elastin breakdown, immune cells, and disease progression. Further understanding of the mechanisms underlying ILC activation and their interaction with elastin peptides could contribute to the development of novel therapeutic strategies for COPD management.
Mots clés
COPD, Elastin peptides, Innate lymphoid cells
Référence
Am J Physiol Lung Cell Mol Physiol. 2024 05 7;: