Coenzyme Q10 suppresses Th17 cells and osteoclast differentiation and ameliorates experimental autoimmune arthritis mice

Jhun, JooYeon; Lee, Jun Young; Byun, Jae-Kyeong; Jeong, Jeong-Hee; Kim, Min Jung; Lee, Jennifer; Jung, Young Ok; Shin, Dongyun; Park, Sung Hwan; Cho, Mi‐La

doi:10.1016/j.imlet.2015.05.012

Cited by 31 publications

(29 citation statements)

References 34 publications

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“…In our previous studies, we demonstrated that CoQ10 has anti-inflammatory functions through the suppression of Th17 cells [15][16][17]. In particular, we showed that CoQ10 inhibited Th17 cells through the suppression of phosphorylated STAT3 (p-STAT3) production [18].…”

Section: Discussionmentioning

confidence: 96%

Liposome/gold hybrid nanoparticle encoded with CoQ10 (LGNP-CoQ10) suppressed rheumatoid arthritis via STAT3/Th17 targeting

Jhun

Moon

Ryu

et al. 2020

Preprint

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Background: Coenzyme Q10 (CoQ10), also known as ubiquinone, is a fat-soluble antioxidant. Although CoQ10 has not been approved as medication by the Food and Drug Administration, it is widely used in dietary supplements. Some studies have shown that CoQ10 has anti-inflammatory effects on various autoimmune disorders.Methods: In this study, we investigated the anti-inflammatory effects of liposome/gold hybrid nanoparticles encoded with CoQ10 (LGNP-CoQ10). Both CoQ10 and LGNP-CoQ10 were administered orally to mice with collagen-induced arthritis (CIA) for 10 weeks. The inflammation pathology of joint tissues of CIA mice was then analyzed using hematoxylin and eosin and Safranin O staining, as well as immunohistochemistry analysis. We obtained immunofluorescence staining images of spleen tissues using confocal microscopy.Results: We found that pro-inflammatory cytokines were significantly decreased in LGNP-CoQ10 injected mice. Th17 cell and phosphorylated STAT3-expressed cell populations were also decreased in LGNP-CoQ10 injected mice. When human peripheral blood mononuclear cells (PBMCs) were treated with CoQ10 and LGNP-CoQ10, the IL-17 expression of PBMCs in the LGNP-CoQ10-treated group was significantly reduced.Conclusion: These results suggest that LGNP-CoQ10 has therapeutic potential for the treatment of rheumatoid arthritis.

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Section: Discussionmentioning

confidence: 96%

Liposome/gold hybrid nanoparticle encoded with CoQ10 (LGNP-CoQ10) suppressed rheumatoid arthritis via STAT3/Th17 targeting

Jhun

Moon

Ryu

et al. 2020

Preprint

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“…Suppression of the in ammatory response with concurrent enhancement of the anti-in ammatory response is the ideal therapeutic approach for patients with autoimmune diseases. Patients with RA have an increased population of Th17 cells and an elevated serum level of IL-17 [32,33]; modulation of these components has been reported to exert bene cial effects in several animal models of RA [34,35]. In the context of RA, B cells and plasma cells were previously considered to be limited to the production of autoantibodies, such as anti-rheumatoid factor and anti-citrullinated protein antibodies.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus sakei suppresses collagen-induced arthritis and modulates the differentiation of T helper 17 cells and regulatory B cells

Jhun¹,

Min

Ryu³

et al. 2020

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Background: To evaluate the immunomodulatory effect of Lactobacillus sakei in a mouse model of rheumatoid arthritis (RA) and in human immune cells. Methods: We evaluated whether L. sakei reduced the severity of collagen-induced arthritis (CIA) and modulated interleukin (IL)-17 and IL-10 levels, as well as whether it affected the differentiation of CD4 + T cells and regulatory B cells. We evaluated osteoclastogenesis after culturing bone marrow-derived mononuclear cells with L. sakei. Results: The differentiation of T helper 17 cells and the serum level of IL-17 were suppressed by L. sakei in both human peripheral blood mononuclear cells and mouse splenocytes. The serum level of IL-10 was significantly increased in the L. sakei -treated group, whereas the regulatory T cell population was unchanged. The population of regulatory B cells significantly increased the in L. sakei -treated group. Oral administration of L. sakei reduced the arthritis incidence and score in mice with CIA. Finally, osteoclastogenesis and the mRNA levels of osteoclast-related genes were suppressed in the L. sakei -treated group. Conclusion: L. sakei exerted an anti-inflammatory effect in an animal model of RA, regulated Th17 and regulatory B cell differentiation, and suppressed osteoclastogenesis. Our findings suggest that L. sakei has therapeutic potential for RA.

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“…To the best of our knowledge, this study is the first to provide evidence indicating that Ssu72 may be an effective therapeutic molecule for the treatment of RA. The inhibition of STAT3 activation has been suggested to exacerbate the development of experimental autoimmune arthritis 7, 21 . Additionally, STAT3 activation increases the number of IL-17-producing Th17 cells and exacerbates the development of RA 22, 23 .…”

Section: Discussionmentioning

confidence: 99%

“…Interleukin-17 (IL-17)-secreting CD4 + T (Th17) cells cause auto-inflammation 5 , whereas Treg cells produce immunosuppressive cytokines, such as IL-10, that limit the immune response in RA pathogenesis 6 . Recently, the reciprocal regulation mediated by Th17 and Treg cells has been suggested as a therapeutic strategy for treating RA 7 .…”

Section: Introductionmentioning

confidence: 99%

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Ssu72 attenuates autoimmune arthritis via targeting of STAT3 signaling and Th17 activation

Lee

Kim

Kwon

et al. 2017

Sci Rep

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Signal transducer and activator of transcription 3 (STAT3) orchestrates the differentiation of several cell types, including interleukin-17 (IL-17)-releasing Th17 cells. Dysregulation of Th17 cells results in chronic inflammatory responses. Ssu72 is a C-terminal domain phosphatase required for transcriptional regulation. However, the mechanism by which Ssu72 affects STAT3 activation and Th17 cell differentiation is unclear. Here, we found that Ssu72 overexpression suppresses STAT3 activation and Th17 cell responses in vitro. A systemic infusion of Ssu72 attenuates experimental autoimmune arthritis by reducing STAT3 activity and the differentiation of Th17 cells. It also reduces joint destruction, serum immunoglobulin concentrations and osteoclastogenesis but increases the number of marginal zone B cells and B10 cells. These effects are associated with reduced p-STAT3 levels and the suppression of Th17 cell formation in vivo. Based on these data, Ssu72 is related to STAT3 activation and the inflammatory response; and Ssu72 overexpression in T-cell-mediated immunity has potential utility for the treatment of autoimmune arthritis.

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Coenzyme Q10 suppresses Th17 cells and osteoclast differentiation and ameliorates experimental autoimmune arthritis mice

Cited by 31 publications

References 34 publications

Liposome/gold hybrid nanoparticle encoded with CoQ10 (LGNP-CoQ10) suppressed rheumatoid arthritis via STAT3/Th17 targeting

Liposome/gold hybrid nanoparticle encoded with CoQ10 (LGNP-CoQ10) suppressed rheumatoid arthritis via STAT3/Th17 targeting

Lactobacillus sakei suppresses collagen-induced arthritis and modulates the differentiation of T helper 17 cells and regulatory B cells

Ssu72 attenuates autoimmune arthritis via targeting of STAT3 signaling and Th17 activation

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