The effects of cholesterol lowering drugs on vitamin D status in familial hypercholesterolemia patients

Background: Familial high blood cholesterol (hypercholesterolemia) is a common disease that involves many complications for patients. The aim of this study is to investigate the effects of cholesterol-lowering drugs (Gemfibrozil and Atorvastatin) on the level of serum Vitamin D.Materials and methods: In this study, the 25-hydroxy vitamin D levels were evaluated in 65 women between 30-55 years of age. After receiving drug information of patients, cholesterol-lowering medication; Gemfibrozil and Atorvastatin were prescribed by a specialist, then vitamin D and cholesterol levels were measured following 9 month treatment. Also 30 patients consumed vitamin D supplements plus medicine regularly.Results: In the first stage, vitamin D levels in subjects are quite normal but their cholesterol levels were higher than normal. In the second stage, vitamin D levels were measured after 9 months use of Gemfibrozil and Atorvastatin. Accordingly, cholesterol levels decreased significantly due to the use of blood cholesterol-lowering drugs (p=0.021). Also, in this stage the level of vitamin D showed a severe and significant reduction (p=0.041). However, there were no significant reductions in vitamin D in 30 women who consumed vitamin D supplements plus medicine (p=0.073).Conclusion: It seems that taking cholesterol-lowering medicines have reduced the amount of vitamin D. With long-term use of medications, bone diseases such as osteoporosis can be predicted in these individuals. Therefore, taking supplements and food rich in vitamin D during the use of these drugs is recommended

Mechanisms of Dysregulated Humoral and Cellular Immunity by SARS-CoV-2

The current coronavirus disease 2019 (COVID-19) pandemic, a disease caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), was first identified in December 2019 in China, and has led to thousands of mortalities globally each day. While the innate immune response serves as the first line of defense, viral clearance requires activation of adaptive immunity, which employs B and T cells to provide sanitizing immunity. SARS-CoV-2 has a potent arsenal of mechanisms used to counter this adaptive immune response through processes, such as T cells depletion and T cell exhaustion. These phenomena are most often observed in severe SARS-CoV-2 patients, pointing towards a link between T cell function and disease severity. Moreover, neutralizing antibody titers and memory B cell responses may be short lived in many SARS-CoV-2 patients, potentially exposing these patients to re-infection. In this review, we discuss our current understanding of B and T cells immune responses and activity in SARS-CoV-2 pathogenesis

Early growth response 2 and Egr3 are unique regulators in immune system

The immune system is evolved to defend the body against pathogens and is composed of thousands of complicated and intertwined pathways, which are highly controlled by processes such as transcription and repression of cellular genes. Sometimes the immune system malfunctions and a break down in self-tolerance occurs. This lead to the inability to distinguish between self and non-self and cause attacks on host tissues, a condition also known as autoimmunity, which can result in chronic debilitating diseases. Early growth response genes are family of transcription factors comprising of four members, Egr1, Egr2, Egr3 and Egr4. All of which contain three cyc2-His2 zinc fingers. Initially, Egr2 function was identified in the regulation of peripheral nerve myelination, hindbrain segmentation. Egr3, on the other hand, is highly expressed in muscle spindle development. Egr2 and Egr3 are induced due to the antigen stimulation and this signaling is implemented through the B and T cell receptors in the adaptive immunity. T cell receptor signaling plays a key role in Egr 2 and 3 expressions via their interaction with NFAT molecules. Egr 2 and 3 play a crucial role in regulation of the immune system and their involvement in B and T cell activation, anergy induction and preventing the autoimmune disease has been investigated. The deficiency of these transcription factors has been associated to deficient Cbl-b expression, a resistant to anergy phenotype, and expression of effector and activated T cells