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Human adipose-derived mesenchymal stem cells attenuate collagen antibody-induced autoimmune arthritis by inducing expression of FCGIIB receptors.

Abstract

BACKGROUND

Adipose-derived stem cells (ASCs) are mesenchymal stem cells (MSCs) derived from adipose tissue. MSCs have multiple properties including anti-inflammatory and immunomodulatory effects in various disease models and human diseases. However, the mechanisms underlying this wide range of effects need to be explored.

METHODS

Collagen antibody-induced arthritis (CAIA) is a unique model in which arthritis is rapidly and strongly induced. ASCs were intraperitoneally infused into CAIA mice before or after arthritis induction. The serum levels of various cytokines, adipokines, and chemokines were measured. The expression of FC gamma receptors (FCGRs) was investigated in peritoneal macrophages ex vivo. RAW264.7 cells and ASCs were co-cultured to elucidate the direct and indirect role of ASCs on FCGR expression.

RESULTS

ASCs attenuated arthritis in CAIA mice. Serum levels of tumor necrosis factor α, interleukin (IL)-15, resistin, and leptin were reduced in ASC-treated CAIA mice, whereas serum levels of IL-6 and adiponectin were not affected. In peritoneal macrophages isolated from ASC-treated mice, expression of FCGRIIB, which is immunoinhibitory, was higher than that of FCGRI. Co-culture of ASCs with RAW264.7 cells modulated the expression of FCGRs. The expression patterns and timings of peak expression differed among FCGRs. Expression of FCGRIIB was higher and peaked earlier than that of FCGRI. FCGRIII expression was not affected by this co-culture.

CONCLUSIONS

This is a study to show that ASCs have anti-arthritic effects in CAIA mice. Modulation of FCGRs by ASCs might be a therapeutic mechanism in this antibody-associated arthritis model.

Authors+Show Affiliations

CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. yallashung@gmail.com.CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. kykang@catholic.ac.kr. Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, 137-040, South Korea. kykang@catholic.ac.kr.CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. starbio98@gmail.com.CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. ilovehyelin@gmail.com.CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. llyerill0114@gmail.com.CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. narae5322@gmail.com.CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. juryunkim1@gmail.com.CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. pobi28@catholic.ac.kr. Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, 137-040, South Korea. pobi28@catholic.ac.kr.Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, 137-040, South Korea. rapark@catholic.ac.kr.CiSTEM Laboratory, Convergent Research Consortium for Immunologic Disease, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea. juji@catholic.ac.kr. Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, 137-040, South Korea. juji@catholic.ac.kr.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26210906

Citation

Yi, Hyoju, et al. "Human Adipose-derived Mesenchymal Stem Cells Attenuate Collagen Antibody-induced Autoimmune Arthritis By Inducing Expression of FCGIIB Receptors." BMC Musculoskeletal Disorders, vol. 16, 2015, p. 170.
Yi H, Kang KY, Kim Y, et al. Human adipose-derived mesenchymal stem cells attenuate collagen antibody-induced autoimmune arthritis by inducing expression of FCGIIB receptors. BMC Musculoskelet Disord. 2015;16:170.
Yi, H., Kang, K. Y., Kim, Y., Jung, H., Rim, Y. A., Park, N., ... Ju, J. H. (2015). Human adipose-derived mesenchymal stem cells attenuate collagen antibody-induced autoimmune arthritis by inducing expression of FCGIIB receptors. BMC Musculoskeletal Disorders, 16, p. 170. doi:10.1186/s12891-015-0634-y.
Yi H, et al. Human Adipose-derived Mesenchymal Stem Cells Attenuate Collagen Antibody-induced Autoimmune Arthritis By Inducing Expression of FCGIIB Receptors. BMC Musculoskelet Disord. 2015 Jul 27;16:170. PubMed PMID: 26210906.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human adipose-derived mesenchymal stem cells attenuate collagen antibody-induced autoimmune arthritis by inducing expression of FCGIIB receptors. AU - Yi,Hyoju, AU - Kang,Kwi Young, AU - Kim,Youngkyun, AU - Jung,Hyerin, AU - Rim,Yeri Alice, AU - Park,Narae, AU - Kim,Juryun, AU - Jung,Seung Min, AU - Park,Sung-Hwan, AU - Ju,Ji Hyeon, Y1 - 2015/07/27/ PY - 2015/03/12/received PY - 2015/07/14/accepted PY - 2015/7/27/entrez PY - 2015/7/27/pubmed PY - 2016/4/2/medline SP - 170 EP - 170 JF - BMC musculoskeletal disorders JO - BMC Musculoskelet Disord VL - 16 N2 - BACKGROUND: Adipose-derived stem cells (ASCs) are mesenchymal stem cells (MSCs) derived from adipose tissue. MSCs have multiple properties including anti-inflammatory and immunomodulatory effects in various disease models and human diseases. However, the mechanisms underlying this wide range of effects need to be explored. METHODS: Collagen antibody-induced arthritis (CAIA) is a unique model in which arthritis is rapidly and strongly induced. ASCs were intraperitoneally infused into CAIA mice before or after arthritis induction. The serum levels of various cytokines, adipokines, and chemokines were measured. The expression of FC gamma receptors (FCGRs) was investigated in peritoneal macrophages ex vivo. RAW264.7 cells and ASCs were co-cultured to elucidate the direct and indirect role of ASCs on FCGR expression. RESULTS: ASCs attenuated arthritis in CAIA mice. Serum levels of tumor necrosis factor α, interleukin (IL)-15, resistin, and leptin were reduced in ASC-treated CAIA mice, whereas serum levels of IL-6 and adiponectin were not affected. In peritoneal macrophages isolated from ASC-treated mice, expression of FCGRIIB, which is immunoinhibitory, was higher than that of FCGRI. Co-culture of ASCs with RAW264.7 cells modulated the expression of FCGRs. The expression patterns and timings of peak expression differed among FCGRs. Expression of FCGRIIB was higher and peaked earlier than that of FCGRI. FCGRIII expression was not affected by this co-culture. CONCLUSIONS: This is a study to show that ASCs have anti-arthritic effects in CAIA mice. Modulation of FCGRs by ASCs might be a therapeutic mechanism in this antibody-associated arthritis model. SN - 1471-2474 UR - https://www.unboundmedicine.com/medline/citation/26210906/Human_adipose_derived_mesenchymal_stem_cells_attenuate_collagen_antibody_induced_autoimmune_arthritis_by_inducing_expression_of_FCGIIB_receptors_ L2 - https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-015-0634-y DB - PRIME DP - Unbound Medicine ER -