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Articles

Vitamin D supplementation ameliorates arthritis but does not alleviates renal injury in pristane-induced lupus model

ORCID Icon, , , , , , , , & show all
Pages 69-77 | Received 12 Jan 2019, Accepted 21 Apr 2019, Published online: 15 May 2019
 

Abstract

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.

Acknowledgments

We thank the employees of Unidade de Experimentação Animal (UEA-HCPA).

Ethics approval

The present study was approved by the Animal Ethics Committee of Hospital de Clínicas de Porto Alegre (HCPA, Porto Alegre, RS, Brazil) and was conducted in accordance with National Institutes of Health guidelines.

Disclosure statement

The authors declare that they have no competing interests.

Additional information

Funding

This study was supported by Research Incentive Fund (FIPE/HCPA) under Grant (n° 17-0011); Conselho Nacional de Desenvolvimento Científico e Tecnológico Universal MCTI/CNPQ under Grant (n° 14/2014) and Research Support Fund of Sociedade de Reumatologia do Rio Grande do Sul. We acknowledge the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Brazil, for a scholarship offered to Eduarda Correa Freitas.

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