Vitamin D3 alleviates RA fatigueThe effects of vitamin D supplementation on disease activity and fatigue in Libyan rheumatoid arthritis patients.
We conducted a study to see how vitamin D3 supplementation affects rheumatoid arthritis (RA), particularly focusing on disease activity and fatigue. In our research design, we organized a randomized clinical trial at rheumatology clinics in Tripoli, Libya, involving patients who were already on conventional disease-modifying antirheumatic drugs (DMARDs).
Participants were split into two groups: one group received a weekly boost of 50,000 IU of vitamin D3, while the other group continued their treatment without any vitamin D3 supplementation. Over a period of 12 weeks, we monitored changes in their symptoms and overall well-being.
Our results revealed something quite remarkable. The group taking vitamin D3 reported notable improvements in fatigue levels compared to those who did not receive the supplement. Specifically, the patients receiving vitamin D3 achieved normal fatigue scores, suggesting their energy levels were significantly better. Additionally, we observed a positive link between higher vitamin D levels and a reduction in fatigue symptoms.
However, there wasn't a significant change in measures of disease activity, indicating that while vitamin D3 can help with fatigue, it may not directly influence the disease's inflammatory aspects in RA patients. Overall, the findings highlight vitamin D3's role in improving the quality of life for individuals battling rheumatoid arthritis through alleviation of fatigue, even when their disease activity remains unchanged.
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Vitamin D3 reduces rheumatoid arthritis inflammation1,25-Dihydroxyvitamin D regulates macrophage activation through FBP1/PKR and ameliorates arthritis in TNF-transgenic mice.
We investigated the role of 1,25-Dihydroxyvitamin D, commonly known as vitamin D3, in managing rheumatoid arthritis (RA). Our study focused on how this vitamin influences macrophage activation, especially in patients with RA.
We found that vitamin D3 has a unique ability to suppress M1 macrophage polarization, a process that intensifies inflammation and is linked to RA symptoms. The treatment reduced levels of various inflammatory markers in macrophages, which are crucial players in our immune response.
In controlled experiments using THP-1 cells (a type of human immune cell), vitamin D3 enhanced the expression of fructose-1,6-bisphosphatase 1 (FBP1). This interaction was significant because FBP1 helps manage the degradation of another protein called PKR, which is involved in the inflammatory response.
By interacting with FBP1 and PKR, vitamin D3 diminishes the inflammatory activity of macrophages, suggesting a pathway for reducing arthritis symptoms. We also observed promising effects in TNF-transgenic mice, where vitamin D3 treatment alleviated arthritic manifestations and promoted a healthier macrophage profile in cells taken from swollen joints.
Overall, our findings affirm the potential of vitamin D3 as a beneficial treatment option for individuals struggling with rheumatoid arthritis.
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20(OH)D3 shows anti-arthritis potential20-Hydroxyvitamin D3, a Secosteroid Produced in Humans, Is Anti-Inflammatory and Inhibits Murine Autoimmune Arthritis.
We explored the effects of 20-hydroxyvitamin D3 (20(OH)D3) on rheumatoid arthritis (RA) in a mouse model. Unlike vitamin D3, which can have harmful effects on the body's calcium levels, 20(OH)D3 offers a noncalcemic alternative that shows promise for chronic treatment of RA.
Our findings demonstrated that 20(OH)D3 significantly suppressed clinical signs of arthritis and reduced joint damage. We observed a decrease in harmful lymphocyte subsets, such as CD4 T cells and CD19 B cells, which are responsible for inflammatory responses in RA. Notably, treatment with 20(OH)D3 resulted in a better balance of regulatory T cells compared to other T cell types, and also a reduction in anti-CII antibodies, critical players in joint damage.
The results of this study suggest that by lowering pro-inflammatory cytokines and antibodies, 20(OH)D3 effectively shields the cartilage and bone from destruction. This positions 20(OH)D3 as a potential candidate for treating RA and possibly other autoimmune disorders, warranting further investigation.
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Calcitriol improves immune function in RACalcitriol Treated Mesenchymal Stem Cells Modulated Immune Response in Collagen-Induced Rheumatoid Arthritis in BALB/c Mice.
We investigated how calcitriol, a form of vitamin D3, influences the immune response in rheumatoid arthritis (RA). In this study, rheumatoid arthritis was induced in BALB/c mice, allowing us to assess the effectiveness of calcitriol-treated mesenchymal stem cells (MSCs) compared to untreated ones. This involved dividing the mice into three groups: one without treatment, one receiving untreated MSCs, and the last treated with calcitriol-exposed MSCs.
Our findings showed that calcitriol treatment significantly improved the regulatory functions of immune cells, particularly splenocytes. In particular, we observed enhanced safety and reduced levels of inflammatory mediators associated with RA. Furthermore, the production of cytokines like IL-4, IL-10, and TGF-β increased, while INF-γ and IL-17 levels decreased in animals treated with calcitriol. This suggests that vitamin D3 could play a promising role in moderating the immune response in RA patients.
Overall, our study highlights the potential of calcitriol in creating effective treatment pathways for rheumatoid arthritis, addressing existing challenges in managing this chronic inflammatory condition.
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Vitamin D3 and arthritis management1,25-Dihydroxyvitamin D3 and 20-Hydroxyvitamin D3 Upregulate LAIR-1 and Attenuate Collagen Induced Arthritis.
We aimed to understand how vitamin D3, both in its active form (1,25-dihydroxyvitamin D3) and a non-calcemic variant (20-hydroxyvitamin D3), influences rheumatoid arthritis. Using a collagen-induced arthritis model in mice, we compared the severity of arthritis in vitamin D-deficient versus normal diet groups.
Our findings indicated that mice with vitamin D deficiency experienced more severe arthritis symptoms characterized by higher levels of inflammatory cytokines produced by T cells. However, when we cultured these T cells with 20(OH)D3, there was a notable suppression of those inflammatory responses.
A significant discovery was that both forms of vitamin D3 led to an increase in LAIR-1, a natural receptor that inhibits immune responses. We noted that activating LAIR-1 with specific antibodies also reduced arthritis symptoms. Interestingly, treatment with vitamin D was effective in mice that had LAIR-1 but not in those lacking this receptor, suggesting LAIR-1 plays a crucial role in how vitamin D helps regulate inflammation.
Overall, our data support the idea that vitamin D, particularly the non-calcemic 20(OH)D3, can be a promising option in treating autoimmune diseases like rheumatoid arthritis, leveraging its effects on LAIR-1.
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