| Title: |
Differences in the inflammatory response and corticoid responsiveness of human lung macrophages and parenchymal explants exposed to cigarette smoke extracts |
| Authors: |
Brollo, M.; Marquant, Q.; Salvator, H.; Cohen, J.; Glorion, M.; Ferré, A.; Dres, M.; Roche, N.; Grassin-Delyle, S.; Devillier, P. |
| Contributors: |
UFR Sciences de la santé Simone Veil (UVSQ Santé); Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Saclay; Hôpital Foch Suresnes; Neurophysiologie Respiratoire Expérimentale et Clinique (UMRS 1158); Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU); Université Paris 13 (UP13); Université Paris Cité (UPCité) |
| Source: |
https://hal.science/hal-05236262 ; 2025. |
| Publisher Information: |
CCSD |
| Publication Year: |
2025 |
| Collection: |
Université de Versailles Saint-Quentin-en-Yvelines: HAL-UVSQ |
| Subject Terms: |
Parenchyma; Inflammatory response; Human lung; [SDV]Life Sciences [q-bio] |
| Description: |
International audience ; Smoking is the main cause of chronic obstructive pulmonary disease and is associated with corticosteroid resistance. Giventhe paucity of data on human lung preparations, macrophages (LMs) and parenchymal explants (LPEs) were exposed tocigarette smoke extract (CSE) in the presence or absence of lipopolysaccharide (LPS). Moreover, LMs and LPEs were treatedwith budesonide prior exposure to CSE or LPS. The levels of cytokines (TNF-α and IL-6) and chemokines (CCL2, CCL4,CXCL1, CXCL5, and CXCL8) in the supernatants were measured using ELISAs. In LMs, exposure to CSE for 24 h wasnot associated with significant difference in the production of cytokines and chemokines, with the notable exception of greaterCXCL8 production. The results were generally the same for LPEs. CSE exposure did not potentiate the LPS-induced productionof the cytokines and chemokines and even tended to reduce this production in LMs and LPEs. Lastly, CSE exposure inhibitedbudesonide’s anti-inflammatory activity in LMs but not in LPEs. The present results extend the literature data on thecigarette smoke’s in vitro inflammatory effects and its inhibition of corticosteroid efficacy in human lung preparations. Ourfindings question the relevance of these lung preparations with regard to the long-term toxicity of smoking and the corticosteroidresistance observed in smokers and in patients with COPD. |
| Document Type: |
report |
| Language: |
English |
| DOI: |
10.22541/au.174282481.17279538/v1 |
| Availability: |
https://hal.science/hal-05236262; https://hal.science/hal-05236262v1/document; https://hal.science/hal-05236262v1/file/1280090.pdf; https://doi.org/10.22541/au.174282481.17279538/v1 |
| Rights: |
https://about.hal.science/hal-authorisation-v1/ ; info:eu-repo/semantics/OpenAccess |
| Accession Number: |
edsbas.DD1852C4 |
| Database: |
BASE |