Alteration of immunophenotype of human macrophages and monocytes after exposure to cigarette smoke.
Aged
Aged, 80 and over
Cigarette Smoking
/ adverse effects
Cytokines
/ metabolism
Female
Humans
Inflammation Mediators
/ metabolism
Macrophages
/ immunology
Male
Middle Aged
Monocytes
/ immunology
Pulmonary Disease, Chronic Obstructive
/ etiology
Risk Factors
Smoke
/ adverse effects
Nicotiana
/ adverse effects
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
30 07 2020
30 07 2020
Historique:
received:
05
03
2020
accepted:
29
06
2020
entrez:
1
8
2020
pubmed:
1
8
2020
medline:
7
1
2021
Statut:
epublish
Résumé
Cigarette smoke exposure (CS) is the main risk factor for chronic obstructive pulmonary disease (COPD). Macrophages have an important role in COPD because they release pro-inflammatory and anti-inflammatory cytokines. The present study's we investigate the functional changes in macrophages and monocytes exposed to cigarette smoke extract (CSE). Herein, using human monocyte-derived macrophages (MDMs) from healthy donors and we found that CSE was not associated with significant changes in the production of pro inflammatory cytokines by MDMs. In contrast, exposure to CSE suppressed the production of IL-6 and Gro-a/CXCL1 by LPS-stimulated-MDMs, but had an additive effect on the release of IL-8/CXCL8 and MCP1/CCL2. However, CSE exposure was associated with greater production, TARC/CCL-17 and CCL22/MDC. Moreover, MDMs displayed a lower uptake capacity after CSE exposure. We identify, for what is to our knowledge the first time that monocytes from patients with COPD produced less IL-8/CXCL8 and Gro-α/CXCL1 after LPS stimulation and produced higher levels of TARC/CCL17 and MDC/CCL-22 after IL-4 stimulation. Our present results highlighted a skewed immune response, with an imbalance in M1 vs. M2 cytokine production. In conclusion, exposure to CS has contrasting, multifaceted effects on macrophages and monocytes. Our data may provide a better understanding of the mechanisms underlying COPD.
Identifiants
pubmed: 32732964
doi: 10.1038/s41598-020-68753-1
pii: 10.1038/s41598-020-68753-1
pmc: PMC7393094
doi:
Substances chimiques
Cytokines
0
Inflammation Mediators
0
Smoke
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
12796Références
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