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Vitamin D supplementation ameliorates arthritis but does not alleviates renal injury in pristane-induced lupus model.
Autoimmunity ( IF 3.3 ) Pub Date : 2019-05-16 , DOI: 10.1080/08916934.2019.1613383
Eduarda Correa Freitas 1, 2, 3 , Thaís Evelyn Karnopp 1, 2, 3 , Jordana Miranda de Souza Silva 1, 2, 3 , Rafaela Cavalheiro do Espírito Santo 1, 2, 3 , Thales Hein da Rosa 1, 3 , Mayara Souza de Oliveira 4 , Fabiany da Costa Gonçalves 1 , Francine Hehn de Oliveira 5 , Pedro Guilherme Schaefer 5 , Odirlei André Monticielo 1, 3
Affiliation  

Systemic lupus erythematosus (SLE) is a multifactorial and autoimmune inflammatory disease with pleomorphic clinical manifestations involving different organs and tissues. The study of different murine models has provided a better understanding of these autoimmune phenomena. Pristane-induced lupus represents a suitable model to study factors that could influence the induction and/or progression of SLE, including genetic factors. The objective of the present study was to evaluate the development and evolution of SLE after vitamin D supplementation in PIL model. Here, we evaluated the effects of vitamin D supplementation in model of pristane-induced SLE in female BALB/c mice. The animals were randomly divided into three groups: control group (CO), pristane-induced lupus group (PIL) and pristane-induced lupus group plus vitamin D (VD). Lupus was induced in PIL and VD groups using pristane. PIL group showed arthritis and kidney injury, characterized by increased proteinuria, glomerular mesangial expansion and inflammation. Moreover, PIL model showed increased levels of IL-6, TNF-α and IFN-γ in serum. We observed that treatment with vitamin D improved arthritis through reduced of incidence and arthritis clinical score and edema, but does not influenced renal injury. Treatment with vitamin D was not able to reduce proteinuria levels, decrease mesangial hypercellularity or IgG and IgM deposition in the kidney. Vitamin D supplementation did not alter IL-6, TNF-α, IL-2 and IL-4, but reduce IFN-γ. These results support that the role of vitamin D may be different depending on acting site, what could explain different responses according clinical phenotype. Therefore, further investigations of vitamin D are needed to explore the supplement dosage, timing, and the molecular basis in SLE.

中文翻译:

补充维生素D可以改善关节炎,但不能减轻在rist烷诱导的狼疮模型中的肾脏损伤。

系统性红斑狼疮(SLE)是一种多因素和自身免疫性炎症性疾病,具有涉及不同器官和组织的多形性临床表现。对不同小鼠模型的研究为这些自身免疫现象提供了更好的理解。rist烷诱导的狼疮代表一种合适的模型,用于研究可能影响SLE诱导和/或进展的因素,包括遗传因素。本研究的目的是评估PIL模型中补充维生素D后SLE的发展和演变。在这里,我们评估了补充维生素D在雌性BALB / c小鼠的rist烷诱导的SLE模型中的作用。将动物随机分为三组:对照组(CO),p烷诱导的狼疮组(PIL)和p烷诱导的狼疮组加维生素D(VD)。使用rist烷在PIL和VD组中诱发狼疮。PIL组表现为关节炎和肾脏损伤,其特征在于蛋白尿增加,肾小球系膜扩张和炎症。而且,PIL模型显示血清中IL-6,TNF-α和IFN-γ水平升高。我们观察到,维生素D的治疗通过降低发病率和降低关节炎的临床评分和水肿改善了关节炎,但并未影响肾脏损伤。维生素D的治疗不能降低蛋白尿水平,不能减少肾小球系膜细胞过多或IgG和IgM沉积。补充维生素D不会改变IL-6,TNF-α,IL-2和IL-4,但会降低IFN-γ。这些结果支持维生素D的作用可能因作用部位而异,这可以根据临床表型解释不同的反应。因此,
更新日期:2019-11-01
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