Differences in the Inflammatory Response and Corticoid Responsiveness of Human Lung Macrophages and Parenchymal Explants Exposed to Cigarette Smoke Extracts
2025
Brollo, Marion | Marquant, Quentin | Salvator, Hélène | Cohen, Justine | Glorion, Matthieu | Ferré, Alexis | Dres, Martin | Roche, Nicolas | Grassin-Delyle, Stanislas | Devillier, Philippe | Virologie et Immunologie Moléculaires (VIM (UR 0892)) ; Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Saclay-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE) | Service de pneumologie [Hôpital Foch] ; Hôpital Foch [Suresnes] | UFR Sciences de la santé Simone Veil (UVSQ Santé) ; Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Saclay | Hôpital Foch [Suresnes] | Centre Hospitalier de Versailles André Mignot (CHV) | Equipe de Statistique Appliquée (UMRS 1158) (ESA) ; Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris) ; Université Paris Sciences et Lettres (PSL)-Université Paris Sciences et Lettres (PSL)-Neurophysiologie Respiratoire Expérimentale et Clinique (UMRS 1158) ; Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU) | CHU Pitié-Salpêtrière [AP-HP] ; Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU) | Institut Cochin (IC UM3 (UMR 8104 / U1016)) ; Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité) | Infection et inflammation (2I) ; Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM)
International audience
Mostrar más [+] Menos [-]Inglés. Smoking is the main cause of chronic obstructive pulmonary disease (COPD) and is associated with corticosteroid resistance. Given the paucity of data on human lung preparations, macrophages (LMs), and parenchymal explants (LPEs) were exposed to cigarette smoke extracts (CSE) in the presence or absence of lipopolysaccharide (LPS). Moreover, LMs and LPEs were treated with budesonide prior exposure to CSE or LPS. The levels of cytokines (TNF-α, IL-6) and chemokines (CCL2, CCL4, CXCL1, CXCL5, and CXCL8) in the supernatants were measured using ELISAs. In LMs, exposure to CSE was not associated with significant difference in the production of cytokines and chemokines, with the notable exception of greater CXCL8 production. The results were generally the same for LPEs. CSE exposure did not potentiate the LPS-induced production of the cytokines and chemokines and even tended to reduce this production in LMs and LPEs. Lastly, CSE exposure inhibited budesonide's anti-inflammatory activity in LMs but not in LPEs. This study extends the data on the CSE inflammatory effects and its inhibition of corticosteroid efficacy in human lung preparations. Our findings question the relevance of these preparations with regard to the long-term toxicity of smoking and the corticosteroid resistance observed in smokers and in patients with COPD.
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