Oral Microbiota and Immune System Crosstalk: A Translational Research.
clinical biochemistry
clinical microbiology
immune system
lymphocytes
macrophage polarization
microbiota
oral pathology
oral-systemic disease
periodontal disease
translational research
Journal
Biology
ISSN: 2079-7737
Titre abrégé: Biology (Basel)
Pays: Switzerland
ID NLM: 101587988
Informations de publication
Date de publication:
16 Jun 2020
16 Jun 2020
Historique:
received:
07
05
2020
revised:
10
06
2020
accepted:
12
06
2020
entrez:
21
6
2020
pubmed:
21
6
2020
medline:
21
6
2020
Statut:
epublish
Résumé
Oral pathogens may exert the ability to trigger differently the activation of local macrophage immune responses, for instance In healthy individuals vs. periodontal disease patients' blood samples, the differentiation process from monocyte to M1 and M2 was conducted using two typical growth factors, the granulocyte/macrophage colony stimulating factor (GM-CSF) and the macrophage colony stimulating factor (M-CSF). In contrast with the current literature our outcomes showed a noticeable increase of macrophage polarization from healthy individuals vs. periodontal patients. The biological and clinical significance of these data was discussed. Our translational findings showed a significant variance between control versus periodontal disease groups in M1 and M2 marker expression within the second group significantly lower skews differentiation of M2-like macrophages towards an M1-like phenotype. Macrophage polarization in periodontal tissue may be responsible for the development and progression of inflammation-induced periodontal tissue damage, including alveolar bone loss, and modulating macrophage function may be a potential strategy for periodontal disease management.
Sections du résumé
BACKGROUND
BACKGROUND
Oral pathogens may exert the ability to trigger differently the activation of local macrophage immune responses, for instance
METHODS
METHODS
In healthy individuals vs. periodontal disease patients' blood samples, the differentiation process from monocyte to M1 and M2 was conducted using two typical growth factors, the granulocyte/macrophage colony stimulating factor (GM-CSF) and the macrophage colony stimulating factor (M-CSF).
RESULTS
RESULTS
In contrast with the current literature our outcomes showed a noticeable increase of macrophage polarization from healthy individuals vs. periodontal patients. The biological and clinical significance of these data was discussed.
CONCLUSIONS
CONCLUSIONS
Our translational findings showed a significant variance between control versus periodontal disease groups in M1 and M2 marker expression within the second group significantly lower skews differentiation of M2-like macrophages towards an M1-like phenotype. Macrophage polarization in periodontal tissue may be responsible for the development and progression of inflammation-induced periodontal tissue damage, including alveolar bone loss, and modulating macrophage function may be a potential strategy for periodontal disease management.
Identifiants
pubmed: 32560235
pii: biology9060131
doi: 10.3390/biology9060131
pmc: PMC7344575
pii:
doi:
Types de publication
Journal Article
Langues
eng
Références
Nat Immunol. 2013 Oct;14(10):986-95
pubmed: 24048120
J Cell Biochem. 2019 Feb 3;:
pubmed: 30714188
J Biol Chem. 2012 Mar 9;287(11):8468-83
pubmed: 22270361
J Periodontol. 2001 Oct;72(10):1398-406
pubmed: 11699482
Int J Med Sci. 2012;9(8):642-54
pubmed: 23055816
Immunity. 2014 Jul 17;41(1):14-20
pubmed: 25035950
Am J Pathol. 2005 May;166(5):1515-22
pubmed: 15855650
Endocr Metab Immune Disord Drug Targets. 2019;19(3):373-381
pubmed: 30574857
Dent Res J (Isfahan). 2017 Nov-Dec;14(6):395-402
pubmed: 29238378
Endocr Metab Immune Disord Drug Targets. 2020 Apr 06;:
pubmed: 32250234
J Leukoc Biol. 2010 May;87(5):753-64
pubmed: 20051473
Arch Oral Biol. 2018 Dec;96:234-242
pubmed: 28351517
J Clin Periodontol. 2018 Jun;45 Suppl 20:S1-S8
pubmed: 29926489
J Bone Miner Res. 2015 Dec;30(12):2140-9
pubmed: 26531055
Cytokine. 2012 Dec;60(3):793-805
pubmed: 22974529
Front Aging Neurosci. 2017 Oct 10;9:327
pubmed: 29085294
Arch Toxicol. 2006 Jun;80(6):378-81
pubmed: 16307232
Int J Immunopathol Pharmacol. 2009 Jan-Mar;22(1):95-103
pubmed: 19309556
J Biol Regul Homeost Agents. 2018 Mar 26;32(2):433-437
pubmed: 29577711
F1000Prime Rep. 2014 Mar 03;6:13
pubmed: 24669294
J Pathol. 1998 Nov;186(3):281-6
pubmed: 10211117
Front Immunol. 2017 Jun 12;8:691
pubmed: 28659924
J Biol Regul Homeost Agents. 2015 Apr-Jun;29(2):273-81
pubmed: 26122214
Infect Immun. 2005 Feb;73(2):935-43
pubmed: 15664935
Curr Oral Health Rep. 2014 Jun 1;1(2):124-132
pubmed: 24839590
J Periodontal Res. 1989 Mar;24(2):106-12
pubmed: 2524575
Biomedicines. 2020 May 09;8(5):
pubmed: 32397555
J Biol Regul Homeost Agents. 2016 Jul-Sep;30(3):863-866
pubmed: 27655512
Trends Immunol. 2004 Dec;25(12):677-86
pubmed: 15530839
Arch Gynecol Obstet. 2012 May;285(5):1325-9
pubmed: 22113463
J Biol Regul Homeost Agents. 2016 Oct-Dec;30(4):1173-1178
pubmed: 28078871
Am J Pathol. 2008 Apr;172(4):1112-26
pubmed: 18321997
J Cell Physiol. 2013 Jul;228(7):1464-72
pubmed: 23255209
Blood. 2006 Jun 15;107(12):4930-7
pubmed: 16497970
Oncotarget. 2017 Sep 28;8(56):95791-95798
pubmed: 29221167
Inflamm Res. 2016 Jan;65(1):1-11
pubmed: 26467935
Int J Med Sci. 2014 May 01;11(7):674-9
pubmed: 24843315
J Cell Biochem. 2012 Apr;113(4):1292-301
pubmed: 22109698
Open Access Maced J Med Sci. 2018 Oct 20;6(10):1845-1850
pubmed: 30455760
Int J Immunopathol Pharmacol. 2010 Apr-Jun;23(2):677-81
pubmed: 20646367
J Biol Regul Homeost Agents. 2018 Sep-Oct;32(5):1323-1328
pubmed: 30334433
Cutan Ocul Toxicol. 2016;35(2):115-9
pubmed: 26095233
mBio. 2017 Jan 24;8(1):
pubmed: 28119468
In Vivo. 2012 Nov-Dec;26(6):1087-9
pubmed: 23160698
Sci Rep. 2018 Aug 14;8(1):12150
pubmed: 30108299
J Clin Periodontol. 2019 Aug;46(8):830-839
pubmed: 31152604
Circulation. 2002 Feb 19;105(7):861-7
pubmed: 11854128
Stem Cells Int. 2017;2017:3292810
pubmed: 28740512