Influence of vitamin D receptor expression (VDR and TLR) in macrophages in the model of experimental diabetes mellitus

Abstract

Vitamin D is a steroid hormone that acts in several mechanisms physiological (participating in the regulation of calcium homeostasis and immune system) and pathological (type 1 diabetes and tumors). Activation of vitamin D occurs through the effect of UVB rays on the skin with subsequent hydroxylations in liver and kidney. After activation, the interaction occurs with the Vitamin D Receptor (VDR) present within the cells, triggering their biological actions. Type 1 diabetes is an autoimmune disease characterized by the destruction of pancreatic beta (²) cells through the action of B lymphocytes, macrophages, CD4 + and CD8 + T cells that culminates in slow, progressive loss of insulin secretion. Vitamin D acts in different stages of the cascade of immune response. Studies have been demonstrated stimulating phagocytosis of the bacteria by macrophages and suppress the ability of antigen presenting dendritic cells, interfering with the production of interleukins (IL)-10, IL-12, tumor necrosis factor (TNF)-± and interferon (IFN)-³ and expression of Toll-like Receptors (TLR). The aim of this work is to study the relationship between vitamin D intake and hormonal mechanisms (production / release of insulin, PTH), blood glucose and the expression of receptors (VDR and TLR) of washed peritoneal macrophages (LPe) and bronchoalveolar (BAL) and immune response in healthy and diabetic mice. The knowledge of the effects of vitamin D in immunity and type 1 diabetes will allow a gain in quality of life of diabetic patients, allowing better control of the disease, since that hormone replacement therapy is easy to perform and inexpensive. (AU)