Calcitriol inhibits osteoclastogenesis in an inflammatory environment by changing the proportion and function of T helper cell subsets (Th2/Th17).

Tytuł:: Calcitriol inhibits osteoclastogenesis in an inflammatory environment by changing the proportion and function of T helper cell subsets (Th2/Th17).
Autorzy:: Bi CS; State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Department of Periodontology, School of Stomatology, Fourth Military Medical University, Xi'an, China.; Department of Periodontics, Stomatology Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Li X; State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Department of Periodontology, School of Stomatology, Fourth Military Medical University, Xi'an, China.
Qu HL; State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Department of Periodontology, School of Stomatology, Fourth Military Medical University, Xi'an, China.
Sun LJ; State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Department of Periodontology, School of Stomatology, Fourth Military Medical University, Xi'an, China.
An Y; State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Department of Periodontology, School of Stomatology, Fourth Military Medical University, Xi'an, China.
Hong YL; Stomatology Center, Shenzhen Hospital of Southern Medical University, Shenzhen, China.
Tian BM; State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Department of Periodontology, School of Stomatology, Fourth Military Medical University, Xi'an, China.
Chen FM; State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Department of Periodontology, School of Stomatology, Fourth Military Medical University, Xi'an, China.
Źródło:: Cell proliferation [Cell Prolif] 2020 Jun; Vol. 53 (6), pp. e12827. Date of Electronic Publication: 2020 May 13.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: [Oxford, England] : Published for the Cell Kinetics Society, the European Study Group for Cell Proliferation, and the International Cell Cycle Society by Blackwell Scientific Publications, 1991-
MeSH Terms:: Calcitriol/*pharmacology
Osteoclasts/*cytology
Osteogenesis/*drug effects
Th17 Cells/*drug effects
Th2 Cells/*drug effects
Animals ; Cells, Cultured ; Dendritic Cells/immunology ; Inflammation ; Lipopolysaccharides/pharmacology ; Mice ; Mice, Inbred C57BL ; Osteoclasts/metabolism ; Phenotype ; Promoter Regions, Genetic ; RANK Ligand/metabolism ; RAW 264.7 Cells ; Th17 Cells/immunology ; Th2 Cells/immunology
References:: Cell Rep. 2014 Dec 11;9(5):1856-1870. (PMID: 25466255)
J Periodontal Res. 2018 Aug;53(4):622-635. (PMID: 29633265)
J Appl Oral Sci. 2015 May-Jun;23(3):329-55. (PMID: 26221929)
Mol Oral Microbiol. 2018 Feb;33(1):13-21. (PMID: 28845602)
Immunol Lett. 2016 Nov;179:122-130. (PMID: 27717877)
Immunopharmacol Immunotoxicol. 2019 Apr;41(2):185-191. (PMID: 31072166)
Front Immunol. 2019 Apr 24;10:787. (PMID: 31068929)
Med Sci Monit. 2020 Jan 08;26:e918370. (PMID: 31914120)
J Steroid Biochem Mol Biol. 2018 Mar;177:70-76. (PMID: 29146302)
Cytokine. 2017 Nov;99:106-113. (PMID: 28802996)
Immune Netw. 2019 Aug 06;19(4):e27. (PMID: 31501715)
J Nutr Biochem. 2014 Jul;25(7):741-9. (PMID: 24794016)
Allergy. 2017 Feb;72(2):221-231. (PMID: 27138374)
J Clin Periodontol. 2009 Dec;36(12):1011-7. (PMID: 19929954)
Front Pharmacol. 2017 Jul 17;8:470. (PMID: 28769800)
J Clin Invest. 2013 Feb;123(2):866-73. (PMID: 23321670)
J Steroid Biochem Mol Biol. 2019 Apr;188:103-110. (PMID: 30605776)
Oncotarget. 2017 Sep 28;8(48):83419-83431. (PMID: 29137353)
Clin Exp Rheumatol. 2018 Sep-Oct;36(5):798-805. (PMID: 29465363)
J Exp Med. 1998 Dec 7;188(11):2175-80. (PMID: 9841930)
Eur Rev Med Pharmacol Sci. 2015 Jul;19(13):2482-92. (PMID: 26214786)
J Asthma. 2015;52(10):989-95. (PMID: 26333305)
Cochrane Database Syst Rev. 2014 Apr 14;(4):CD000227. (PMID: 24729336)
Periodontol 2000. 2020 Feb;82(1):186-204. (PMID: 31850625)
J Neuroinflammation. 2019 Mar 1;16(1):52. (PMID: 30823934)
Nature. 2003 Feb 13;421(6924):744-8. (PMID: 12610626)
Cell Prolif. 2020 Jun;53(6):e12827. (PMID: 32406154)
J Immunol. 2001 Nov 1;167(9):4974-80. (PMID: 11673504)
Endocrinol Metab Clin North Am. 2017 Dec;46(4):1061-1094. (PMID: 29080635)
Sci Rep. 2016 Jun 16;6:28290. (PMID: 27306570)
J Immunol Res. 2015;2015:615486. (PMID: 26065002)
J Dent Res. 2008 Sep;87(9):817-28. (PMID: 18719207)
J Autoimmun. 2017 Dec;85:78-97. (PMID: 28733125)
Gastroenterology. 2020 Apr;158(5):1359-1372.e9. (PMID: 31917258)
J Steroid Biochem Mol Biol. 2016 Nov;164:239-245. (PMID: 26343449)
Int Immunopharmacol. 2018 Mar;56:339-348. (PMID: 29454234)
Cell Prolif. 2018 Oct;51(5):e12461. (PMID: 29687949)
J Clin Periodontol. 2011 Jun;38(6):509-16. (PMID: 21392046)
Mol Endocrinol. 2008 Jan;22(1):176-85. (PMID: 17885208)
Food Chem Toxicol. 2018 Oct;120:418-429. (PMID: 30048646)
JCI Insight. 2019 Sep 19;4(18):. (PMID: 31487265)
Cytokine. 2015 Sep;75(1):14-24. (PMID: 26044597)
Clin Dev Immunol. 2013;2013:584303. (PMID: 24288552)
Clin Exp Dent Res. 2019 Aug;5(4):377-388. (PMID: 31944625)
J Cell Biochem. 2018 Feb;119(2):2084-2093. (PMID: 28834554)
J Periodontol. 2017 Aug;88(8):788-798. (PMID: 28492360)
J Autoimmun. 2018 Mar;88:50-60. (PMID: 29066221)
J Periodontal Res. 2019 Dec;54(6):612-623. (PMID: 31095745)
Inflammation. 2018 Oct;41(5):1791-1803. (PMID: 29951876)
J Dent (Tehran). 2013 Jan;10(1):23-31. (PMID: 23724200)
Stem Cells. 2019 Dec;37(12):1567-1580. (PMID: 31400241)
J Biol Chem. 2010 Dec 10;285(50):38751-5. (PMID: 20974859)
World J Gastroenterol. 2008 Jun 28;14(24):3897-902. (PMID: 18609716)
Immunol Invest. 2016;45(3):243-54. (PMID: 27019379)
Front Cell Infect Microbiol. 2017 Apr 27;7:140. (PMID: 28497028)
J Periodontol. 2018 Oct;89(10):1249-1261. (PMID: 30030845)
Clin Cases Miner Bone Metab. 2015 May-Aug;12(2):174-7. (PMID: 26604945)
Immunol Res. 2019 Feb;67(1):48-57. (PMID: 30357602)
PLoS One. 2017 Jan 23;12(1):e0169870. (PMID: 28114408)
Grant Information:: 81530050 National Natural Science Foundation of China; 81800971 National Natural Science Foundation of China; 2017KCT-32 Shaanxi Key Scientific and Technological Innovation Team
Contributed Indexing:: Keywords: T helper cells; calcitriol; dendritic cells; immunomodulation; osteoclastogenesis
Substance Nomenclature:: 0 (Lipopolysaccharides)
0 (RANK Ligand)
0 (Tnfsf11 protein, mouse)
FXC9231JVH (Calcitriol)
Entry Date(s):: Date Created: 20200515 Date Completed: 20200706 Latest Revision: 20200706
Update Code:: 20240105
PubMed Central ID:: PMC7309596
DOI:: 10.1111/cpr.12827
PMID:: 32406154
: Czasopismo naukowe

Pełny tekst

Objectives: Previously, we found that by regulating T helper (Th) cell polarization, calcitriol intervention inhibited lipopolysaccharide (LPS)-induced alveolar bone loss in an animal periodontitis model, but the underlying cellular events remain unknown.
Materials and Methods: In this study, mouse Th cells were incubated in an inflammatory environment in the presence of dendritic cells (DCs) and LPS. Then, the potential of the Th cells to undergo Th2/Th17 polarization, the RANKL expression of the polarized Th cells and the subsequent influences of the polarized Th cells on RAW264.7 cell osteoclastogenesis in response to calcitriol administration were assessed. Finally, the effects of calcitriol on antigen presentation by DCs during these cellular events were evaluated.
Results: In response to calcitriol administration, Th cells in an inflammatory environment exhibited an enhanced potential for Th2 polarization along with a decreased potential for Th17 polarization. In addition, RANKL expression in Th17-polarized cells was largely inhibited. Furthermore, inflammation-induced osteoclastogenesis in RAW264.7 cells was suppressed following coculture with calcitriol-treated Th cells. During these cellular events, increased expression of Th2 promoters (such as OX-40L and CCL17) and decreased expression of Th17 promoters (such as IL-23 and IL-6) were found in DCs.
Conclusions: Calcitriol can inhibit osteoclastogenesis in an inflammatory environment by changing the proportion and function of Th cell subsets. Our findings suggest that calcitriol may be an effective therapeutic agent for treating periodontitis.
(© 2020 The Authors. Cell Proliferation published by John Wiley & Sons Ltd.)

Zaloguj się, aby uzyskać dostęp do pełnego tekstu.

Informacja