Synovial fluid monocyte/macrophage subsets and their correlation to patient-reported outcomes in osteoarthritic patients: a cohort study.
Leukocytes
Monocytes/macrophages
Osteoarthritis
PROMs
Synovial fluid
Journal
Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438
Informations de publication
Date de publication:
18 01 2019
18 01 2019
Historique:
received:
07
06
2018
accepted:
17
12
2018
entrez:
20
1
2019
pubmed:
20
1
2019
medline:
17
3
2020
Statut:
epublish
Résumé
Chronic, low-grade inflammation of the synovium (synovitis) is a hallmark of osteoarthritis (OA), thus understanding of OA immunobiology, mediated by immune effectors, is of importance. Specifically, monocytes/macrophages (MΦs) are known to be abundantly present in OA joints and involved in OA progression. However, different subsets of OA MΦs have not been investigated in detail, especially in terms of their relationship with patient-reported outcome measures (PROMs). We hypothesized that levels of synovial fluid (SF) MΦ subsets are indicative of joint function and quality of life in patients with OA, and can therefore serve as biomarkers and therapeutic targets for OA. In this cohort study, synovial fluid leukocytes (SFLs, N = 86) and peripheral blood mononuclear cells (n = 53) from patients with knee OA were characterized. Soluble MΦ receptors and chemokine (sCD14, sCD163, CCL2, CX3CL1) levels were detected in SF using immunoassays. Linear models, adjusted for sex, age and body mass index, were used to determine associations between SF MΦs and soluble factors with PROMs (N = 83). Pearson correlation was calculated to determine correlation between MΦ subsets, T cells and soluble factors. SF MΦs were the most abundant SFLs. Within these, the double-positive CD14 SF MΦ subsets are associated with knee OA PROMs and display an activated phenotype, which may lead to modulation of CD4
Sections du résumé
BACKGROUND
Chronic, low-grade inflammation of the synovium (synovitis) is a hallmark of osteoarthritis (OA), thus understanding of OA immunobiology, mediated by immune effectors, is of importance. Specifically, monocytes/macrophages (MΦs) are known to be abundantly present in OA joints and involved in OA progression. However, different subsets of OA MΦs have not been investigated in detail, especially in terms of their relationship with patient-reported outcome measures (PROMs). We hypothesized that levels of synovial fluid (SF) MΦ subsets are indicative of joint function and quality of life in patients with OA, and can therefore serve as biomarkers and therapeutic targets for OA.
METHODS
In this cohort study, synovial fluid leukocytes (SFLs, N = 86) and peripheral blood mononuclear cells (n = 53) from patients with knee OA were characterized. Soluble MΦ receptors and chemokine (sCD14, sCD163, CCL2, CX3CL1) levels were detected in SF using immunoassays. Linear models, adjusted for sex, age and body mass index, were used to determine associations between SF MΦs and soluble factors with PROMs (N = 83). Pearson correlation was calculated to determine correlation between MΦ subsets, T cells and soluble factors.
RESULTS
SF MΦs were the most abundant SFLs. Within these, the double-positive CD14
CONCLUSION
SF MΦ subsets are associated with knee OA PROMs and display an activated phenotype, which may lead to modulation of CD4
Identifiants
pubmed: 30658702
doi: 10.1186/s13075-018-1798-2
pii: 10.1186/s13075-018-1798-2
pmc: PMC6339358
doi:
Substances chimiques
Chemokines
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
26Subventions
Organisme : Arthritis Society
ID : TAS-YIO-15-321
Pays : International
Organisme : Arthritis Society
ID : TPF-15-123
Pays : International
Références
Bratisl Lek Listy. 2009;110(10):641-6
pubmed: 20017457
Nephrol Dial Transplant. 2000 May;15(5):574-8
pubmed: 10809793
Arthritis Rheum. 1986 Aug;29(8):1039-49
pubmed: 3741515
Arthritis Rheum. 2007 Jan;56(1):147-57
pubmed: 17195217
Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):20602-7
pubmed: 23185004
Ann Clin Biochem. 2013 Nov;50(Pt 6):571-5
pubmed: 23869024
Ann Clin Biochem. 2015 Mar;52(Pt 2):276-82
pubmed: 25005456
Immunol Res. 2012 Sep;53(1-3):41-57
pubmed: 22430559
J Investig Med. 2015 Apr;63(4):626-31
pubmed: 25692263
Best Pract Res Clin Rheumatol. 2010 Feb;24(1):15-26
pubmed: 20129196
Osteoarthritis Cartilage. 2018 Sep;26(9):1247-1256
pubmed: 29753948
Arthritis Rheumatol. 2015 Apr;67(4):956-65
pubmed: 25544994
Nat Rev Rheumatol. 2013 Aug;9(8):485-97
pubmed: 23689231
Arthritis Rheum. 2010 Mar;62(3):647-57
pubmed: 20187160
PLoS One. 2009 Oct 16;4(10):e7475
pubmed: 19834619
Osteoarthritis Cartilage. 2016 Nov;24(11):1867-1874
pubmed: 27262546
Ann Rheum Dis. 2014 Jun;73(6):1067-70
pubmed: 23606704
Osteoarthritis Cartilage. 2017 Mar;25(3):406-412
pubmed: 27746376
Clin Exp Immunol. 2017 Feb;187(2):234-241
pubmed: 27706807
Clin Immunol. 2009 Mar;130(3):338-46
pubmed: 18952503
PLoS One. 2014 Oct 17;9(10):e109775
pubmed: 25329467
Heredity (Edinb). 2005 Sep;95(3):221-7
pubmed: 16077740
Ann Rheum Dis. 2017 May;76(5):914-922
pubmed: 27965260
Ann Rheum Dis. 2018 Feb;77(2):300-308
pubmed: 29191820
Blood. 2000 Jul 1;96(1):218-23
pubmed: 10891454
Osteoarthritis Cartilage. 2012 Dec;20(12):1484-99
pubmed: 22960092
Osteoarthritis Cartilage. 2017 Jul;25(7):1150-1160
pubmed: 28189826
ISRN Orthop. 2012 Aug 30;2012:413105
pubmed: 24977076
PM R. 2012 Dec;4(12):1001-5
pubmed: 23245662
Ann Rheum Dis. 2007 Dec;66(12):1599-603
pubmed: 17491096
J Exp Med. 2017 Jul 3;214(7):1913-1923
pubmed: 28606987
Arthritis Res Ther. 2017 May 19;19(1):103
pubmed: 28526072
Rheumatology (Oxford). 2014 Nov;53(11):2095-9
pubmed: 24939675
Nat Rev Rheumatol. 2010 Nov;6(11):625-35
pubmed: 20924410
Blood. 2011 Sep 22;118(12):e50-61
pubmed: 21803849
Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6232-7
pubmed: 19325128
J Biol Chem. 2010 Dec 24;285(52):40800-8
pubmed: 20959457
Cytometry A. 2012 Oct;81(10):823-34
pubmed: 22837127