Platelet Mediated Inflammation in Coronary Artery Disease with Type 2 Diabetes Patients.
coronary artery disease
hyperglycemia
inflammation
monocytes
platelet
type 2 diabetes
Journal
Journal of inflammation research
ISSN: 1178-7031
Titre abrégé: J Inflamm Res
Pays: New Zealand
ID NLM: 101512684
Informations de publication
Date de publication:
2021
2021
Historique:
received:
29
06
2021
accepted:
19
08
2021
entrez:
22
10
2021
pubmed:
23
10
2021
medline:
23
10
2021
Statut:
epublish
Résumé
Type 2 diabetes mellitus (T2DM) is a well-established risk factor for the development of atherosclerotic coronary artery disease. Platelet hyperactivity and inflammation are associated with the development of coronary artery disease (CAD) in T2DM patients. We investigated the status of immune cells, platelet activation, and platelet-immune cell interactions in T2DM_CAD patients. The study population consisted of four groups of subjects, healthy control (CT, n = 20), T2DM (n = 44), CAD (n = 20) and T2DM_CAD (n = 38). Platelet activation, immunome profiling and platelet-immune cell interactions were analysed by flow cytometry. The circulatory levels of inflammatory cytokines/chemokines were assessed using multiplex assay. Increased platelet activation and increased platelet-immune cell aggregate formation were observed in T2DM and T2DM_CAD groups compared to the control and CAD groups (p < 0.05). Our immunome profile analysis revealed, altered monocyte subpopulations and dendritic cell populations in T2DM, CAD and T2DM_CAD groups compared to the control group (p < 0.05). Furthermore, significantly increased IL-1β, IL-2, IL-4, IL-6, IL-8, IL12p70, IL-13 IL-18, CCL2, and decreased CXCL1, CCL5 levels were observed in T2DM_CAD group compared to the control group. Our ex-vivo study increased platelet-monocyte aggregate formation was observed upon D-glucose exposure in a time and concentration dependent manner. Our data suggests that T2DM, CAD and T2DM_CAD are associated with altered immune cell populations. Furthermore, it has been confirmed that hyperglycemia induces platelet activation and forms platelet-immune cell aggregation which may lead to the release of inflammatory cytokines and chemokines and contribute to the complexity of CAD and type 2 diabetes.
Sections du résumé
BACKGROUND
BACKGROUND
Type 2 diabetes mellitus (T2DM) is a well-established risk factor for the development of atherosclerotic coronary artery disease. Platelet hyperactivity and inflammation are associated with the development of coronary artery disease (CAD) in T2DM patients. We investigated the status of immune cells, platelet activation, and platelet-immune cell interactions in T2DM_CAD patients.
METHODOLOGY
METHODS
The study population consisted of four groups of subjects, healthy control (CT, n = 20), T2DM (n = 44), CAD (n = 20) and T2DM_CAD (n = 38). Platelet activation, immunome profiling and platelet-immune cell interactions were analysed by flow cytometry. The circulatory levels of inflammatory cytokines/chemokines were assessed using multiplex assay.
RESULTS
RESULTS
Increased platelet activation and increased platelet-immune cell aggregate formation were observed in T2DM and T2DM_CAD groups compared to the control and CAD groups (p < 0.05). Our immunome profile analysis revealed, altered monocyte subpopulations and dendritic cell populations in T2DM, CAD and T2DM_CAD groups compared to the control group (p < 0.05). Furthermore, significantly increased IL-1β, IL-2, IL-4, IL-6, IL-8, IL12p70, IL-13 IL-18, CCL2, and decreased CXCL1, CCL5 levels were observed in T2DM_CAD group compared to the control group. Our ex-vivo study increased platelet-monocyte aggregate formation was observed upon D-glucose exposure in a time and concentration dependent manner.
CONCLUSION
CONCLUSIONS
Our data suggests that T2DM, CAD and T2DM_CAD are associated with altered immune cell populations. Furthermore, it has been confirmed that hyperglycemia induces platelet activation and forms platelet-immune cell aggregation which may lead to the release of inflammatory cytokines and chemokines and contribute to the complexity of CAD and type 2 diabetes.
Identifiants
pubmed: 34675593
doi: 10.2147/JIR.S326716
pii: 326716
pmc: PMC8504552
doi:
Types de publication
Journal Article
Langues
eng
Pagination
5131-5147Informations de copyright
© 2021 Johny et al.
Déclaration de conflit d'intérêts
The authors declare no conflicts of interest for this work.
Références
J Hum Hypertens. 2022 Jun;36(6):561-569
pubmed: 33837293
Biomed Res Int. 2016;2016:9060143
pubmed: 27403440
Curr Pharm Des. 2014;20(28):4580-8
pubmed: 24862889
Cell Rep. 2020 May 12;31(6):107615
pubmed: 32402278
J Immunol. 2011 May 1;186(9):5489-96
pubmed: 21430222
Arterioscler Thromb Vasc Biol. 2015 Apr;35(4):763-70
pubmed: 25675999
Cell Metab. 2013 May 7;17(5):695-708
pubmed: 23663738
Nat Rev Immunol. 2019 Dec;19(12):734-746
pubmed: 31501536
Cardiovasc Diabetol. 2018 Nov 2;17(1):141
pubmed: 30388964
J Transl Med. 2019 Jan 24;17(1):17
pubmed: 30674322
Blood. 2014 May 1;123(18):2759-67
pubmed: 24585776
Front Immunol. 2019 Aug 30;10:2035
pubmed: 31543877
Int J Endocrinol. 2011;2011:742719
pubmed: 21869886
J Clin Lab Anal. 2018 Jul;32(6):e22402
pubmed: 29430728
Atherosclerosis. 2014 May;234(1):4-10
pubmed: 24583499
Med Sci Monit. 2019 Mar 03;25:1645-1655
pubmed: 30826813
Compr Physiol. 2015 Jul 1;5(3):1265-80
pubmed: 26140718
J Cell Biol. 2001 Aug 6;154(3):485-90
pubmed: 11489912
PLoS One. 2020 Mar 4;15(3):e0229765
pubmed: 32130282
Diabetes. 2005 Dec;54 Suppl 2:S11-7
pubmed: 16306328
Cardiovasc Diabetol. 2014 Jan 03;13:1
pubmed: 24383855
Int J Cardiol. 2020 Aug 15;313:99-104
pubmed: 32223966
Cardiol Clin. 2014 Aug;32(3):439-55
pubmed: 25091969
Am J Hypertens. 2014 Apr;27(4):571-8
pubmed: 23975222
Diabetes Metab Syndr. 2018 May;12(3):221-225
pubmed: 28988596
J Diabetes Res. 2015;2015:490842
pubmed: 26273671
Diabetes Res Clin Pract. 2019 Nov;157:107843
pubmed: 31518657
Eur Heart J. 2009 Dec;30(24):3048-54
pubmed: 19687162
J Exp Med. 2016 Mar 7;213(3):337-54
pubmed: 26926996
J Leukoc Biol. 2006 Mar;79(3):499-507
pubmed: 29350799
Cardiovasc Diabetol. 2010 Mar 23;9:11
pubmed: 20331890
J Diabetes Res. 2013;2013:184258
pubmed: 23762872
Int Immunopharmacol. 2013 Dec;17(4):1176-84
pubmed: 23810443
Diab Vasc Dis Res. 2019 Sep;16(5):458-465
pubmed: 31046456
Inflammation. 2013 Dec;36(6):1225-31
pubmed: 23715819
Nucleic Acids Res. 2019 Jan 8;47(D1):D607-D613
pubmed: 30476243
Arterioscler Thromb Vasc Biol. 2008 Nov;28(11):1920-7
pubmed: 18723831
Arq Bras Cardiol. 2020 Apr;114(4):692-698
pubmed: 32491018
J Thromb Thrombolysis. 2021 May;51(4):1138-1143
pubmed: 33043416
Biochim Biophys Acta Mol Basis Dis. 2018 Sep;1864(9 Pt B):2901-2912
pubmed: 29864522
Cardiovasc Diabetol. 2018 Aug 31;17(1):122
pubmed: 30170598
Biomed Res Int. 2017;2017:4013685
pubmed: 28349060
Nucleic Acids Res. 2009 Jan;37(1):1-13
pubmed: 19033363
Trends Endocrinol Metab. 2019 Aug;30(8):532-545
pubmed: 31196615
Exp Clin Endocrinol Diabetes. 2008 Mar;116(3):162-6
pubmed: 18213547
Clin Exp Immunol. 2018 Oct;194(1):125-136
pubmed: 30022471
Int J Mol Sci. 2019 Aug 27;20(17):
pubmed: 31461836
Eur Cytokine Netw. 2005 Sep;16(3):177-85
pubmed: 16266856
Transfus Med Hemother. 2016 Mar;43(2):78-88
pubmed: 27226790
Cardiovasc Res. 2007 Sep 1;75(4):793-802
pubmed: 17572401
Front Immunol. 2018 Nov 20;9:2712
pubmed: 30515177
Mediators Inflamm. 2015;2015:435783
pubmed: 25814789
J Physiol Pharmacol. 2016 Apr;67(2):321-8
pubmed: 27226191
Thromb Haemost. 2015 Aug 31;114(3):449-58
pubmed: 26293514
Sci Rep. 2017 Jul 31;7(1):6877
pubmed: 28761077
Can J Cardiol. 2006 Mar 1;22(3):193-7
pubmed: 16520847
Coron Artery Dis. 2006 May;17(3):243-8
pubmed: 16728874
World J Diabetes. 2014 Aug 15;5(4):444-70
pubmed: 25126392
Diabetes Care. 2014 Aug;37(8):2400-3
pubmed: 24879840
PLoS One. 2011;6(10):e25595
pubmed: 22022418
Cardiovasc Diabetol. 2018 Aug 31;17(1):121
pubmed: 30170601
Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7265-70
pubmed: 12756299