Anti-inflammatory effects of cold atmospheric plasma irradiation on the THP-1 human acute monocytic leukemia cell line.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2023
2023
Historique:
received:
21
06
2023
accepted:
15
09
2023
medline:
23
10
2023
pubmed:
18
10
2023
entrez:
18
10
2023
Statut:
epublish
Résumé
Cold atmospheric plasma (CAP) has been studied and clinically applied to treat chronic wounds, cancer, periodontitis, and other diseases. CAP exerts cytotoxic, bactericidal, cell-proliferative, and anti-inflammatory effects on living tissues by generating reactive species. Therefore, CAP holds promise as a treatment for diseases involving chronic inflammation and bacterial infections. However, the cellular mechanisms underlying these anti-inflammatory effects of CAP are still unclear. Thus, this study aimed to elucidate the anti-inflammatory mechanisms of CAP in vitro. The human acute monocytic leukemia cell line, THP-1, was stimulated with lipopolysaccharide and irradiated with CAP, and the cytotoxic effects of CAP were evaluated. Time-course differentiation of gene expression was analyzed, and key transcription factors were identified via transcriptome analysis. Additionally, the nuclear localization of the CAP-induced transcription factor was examined using western blotting. The results indicated that CAP showed no cytotoxic effects after less than 70 s of irradiation and significantly inhibited interleukin 6 (IL6) expression after more than 40 s of irradiation. Transcriptome analysis revealed many differentially expressed genes (DEGs) following CAP irradiation at all time points. Cluster analysis classified the DEGs into four distinct groups, each with time-dependent characteristics. Gene ontology and gene set enrichment analyses revealed CAP-induced suppression of IL6 production, other inflammatory responses, and the expression of genes related to major histocompatibility complex (MHC) class II. Transcription factor analysis suggested that nuclear factor erythroid 2-related factor 2 (NRF2), which suppresses intracellular oxidative stress, is the most activated transcription factor. Contrarily, regulatory factor X5, which regulates MHC class II expression, is the most suppressed transcription factor. Western blotting revealed the nuclear localization of NRF2 following CAP irradiation. These data suggest that CAP suppresses the inflammatory response, possibly by promoting NRF2 nuclear translocation.
Identifiants
pubmed: 37851686
doi: 10.1371/journal.pone.0292267
pii: PONE-D-23-17572
pmc: PMC10584116
doi:
Substances chimiques
NF-E2-Related Factor 2
0
Plasma Gases
0
Interleukin-6
0
Anti-Inflammatory Agents
0
Lipopolysaccharides
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0292267Informations de copyright
Copyright: © 2023 Hirasawa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
Références
Immunology. 2021 May;163(1):3-18
pubmed: 33064842
Biochem Biophys Res Commun. 2018 Sep 10;503(3):2040-2046
pubmed: 30086885
Genome Res. 2019 Aug;29(8):1363-1375
pubmed: 31340985
Immunity. 2008 Oct 17;29(4):565-77
pubmed: 18848473
J Biol Chem. 2015 Mar 13;290(11):6731-50
pubmed: 25589789
Inflamm Allergy Drug Targets. 2012 Apr;11(2):159-68
pubmed: 22280236
Nitric Oxide. 2010 Aug 1;23(1):65-73
pubmed: 20399279
Inflamm Res. 2014 Dec;63(12):1001-12
pubmed: 25369802
J Clin Periodontol. 2018 Jun;45 Suppl 20:S162-S170
pubmed: 29926490
Eur J Immunol. 2004 Jun;34(6):1513-25
pubmed: 15162420
PLoS One. 2016 Aug 18;11(8):e0161482
pubmed: 27536946
Theranostics. 2019 Jan 30;9(4):1066-1084
pubmed: 30867816
Trends Immunol. 2016 Nov;37(11):724-737
pubmed: 27614798
Bioact Mater. 2021 Aug 05;9:428-445
pubmed: 34820581
J Clin Periodontol. 2002 Aug;29(8):705-9
pubmed: 12390567
J Clin Periodontol. 1998 Feb;25(2):134-44
pubmed: 9495612
Gene. 2016 Jun 10;584(1):17-25
pubmed: 26947393
Oxid Med Cell Longev. 2018 Oct 2;2018:1347969
pubmed: 30370001
Innate Immun. 2008 Apr;14(2):99-107
pubmed: 18713726
Int J Mol Sci. 2021 Apr 06;22(7):
pubmed: 33917526
Nat Genet. 2016 Aug;48(8):838-47
pubmed: 27322546
J Biochem. 2010 Jun;147(6):781-92
pubmed: 20410014
Front Microbiol. 2019 Apr 02;10:622
pubmed: 31001215
Gene. 2016 May 1;581(2):152-60
pubmed: 26812355
PLoS One. 2014 Dec 12;9(12):e115107
pubmed: 25501558
EMBO Rep. 2018 Sep;19(9):
pubmed: 30021835
Clin Dev Immunol. 2012;2012:925135
pubmed: 22474485
Antioxid Redox Signal. 2018 Dec 10;29(17):1727-1745
pubmed: 28899199
Cell Syst. 2015 Dec 23;1(6):417-425
pubmed: 26771021
J Immunol. 2021 Aug 1;207(3):913-922
pubmed: 34290107
Surgery. 2009 Aug;146(2):155-65
pubmed: 19628069
Nat Commun. 2016 May 23;7:11624
pubmed: 27211851
Antioxid Redox Signal. 2015 Aug 1;23(4):328-39
pubmed: 26140517
Immune Netw. 2009 Feb;9(1):12-9
pubmed: 20107533
PLoS One. 2015 Oct 13;10(10):e0139903
pubmed: 26461113
Periodontol 2000. 2010 Oct;54(1):53-70
pubmed: 20712633
Mol Oral Microbiol. 2016 Dec;31(6):445-456
pubmed: 26505640
BMC Evol Biol. 2008 Aug 01;8:226
pubmed: 18673564
Int J Mol Sci. 2019 Jul 10;20(14):
pubmed: 31295952
Methods. 2001 Dec;25(4):402-8
pubmed: 11846609
J Biol Chem. 1999 Mar 19;274(12):7611-4
pubmed: 10075645
Oxid Med Cell Longev. 2019 May 19;2019:7071536
pubmed: 31223425
J Periodontal Res. 2020 Aug;55(4):473-487
pubmed: 31960443
Nat Methods. 2012 Jul;9(7):671-5
pubmed: 22930834
Clin Oral Investig. 2020 Sep;24(9):3133-3145
pubmed: 31897708
J Immunol. 2004 May 15;172(10):6185-94
pubmed: 15128806