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Abstract Introduction Vitamin D has important roles as a natural immune modulator via regulating the expression of genes which have been implicated in the pathophysiology of autoimmune diseases. Vitamin D function and its deficiency have been linked to a wide range of metabolic disorders including disorders of calcium metabolism, malignant, cardiovascular, infectious, neuromuscular, and inflammatory diseases. Environmental factors, genetic factors, and epigenetic changes contribute to Behcet's disease (BD) development. The aim of our study was to analyze the expression level and methylation status of the vitamin D receptor (VDR) gene promoter in the peripheral blood mononuclear cells (PBMCs) of patients with BD. Methods In a case‐control study, 48 Iranian Azeri patients with BD and 60 age‐, sex‐ and ethnically‐matched healthy controls were included. Venous blood samples were collected and PBMCs were isolated by Ficoll protocol. The DNA and RNA were subsequently extracted. Promoter methylation levels were evaluated by MeDIP‐quantitative polymerase chain reaction (qPCR). The expression of VDR was evaluated by real‐time PCR. Results The results of quantitative real‐time PCR analysis showed that the level of VDR expression in patients with BD was significantly lower than the control group (P = .013). There was no significant difference in the level of DNA methylation in the BD and control groups (P > .05). As the results show, the expression level of VDR gene was significantly different between female and male in the patient group (P = .001). VDR gene expression was significantly higher in subjects with phlebitis. No correlation was observed between VDR gene expression rate and BD activity. Conclusion VDR gene expression decreased in patients with BD. However, there is no suggestion evidence that the expression level of VDR is regulated by a unique DNA methylation mechanism. No correlation exists between VDR gene expression and BD activity.

Objective: MicroRNAs are ribonucleic acids that are single-stranded and endogenous non-coding acids that regulate gene expression in later stages of the translation process by binding to genomic regulatory sites. miR146a is mostly involved in the regulation of inflammatory systems and another process that role in the innate immune system. In the present review, we have focused on the recent acquisitions about the main role played by mir146a in the control of the immune system and tumorigenesis. The main purpose of this review article is to systematically investigate the mir146a and its role in regulating signaling pathways involved in cancer and the immune system as well as its involved therapeutic methods. Methods: Systematic search of MEDLINE, Web of Science and Cochrane Library was conducted for all comparative studies from 2000 to 2019 with the limitations of the English language. Results: For a notable period of time, researchers have mainly focused on the therapeutic mechanisms of mir146a involved in the modulation of inflammatory and anti-inflammatory genes. We found that levels of mir146a expression were associated with cancer cell metastasis as a dual role (Inhibitory and stimulatory roles). The results of various studies also showed that this microRNA has a therapeutic role through its effects on other gene expressions such as NF-kB, SIRT1, TNF- α and IL-1β and leads to disease control. Conclusion: Knowledge about alterations in mir146a regulation will give a better understanding of the molecular basis for various chronic inflammatory diseases and cancers.

COVID-19 can induce lung inflammation, and inflammatory factors play an essential role in its pathogenesis. This inflammation can be controlled to a great extent by microRNAs (miRs). This study evaluated miR-146a-5p expression levels in the serum of patients with COVID-19 and their association with the expression of interleukin (IL)-18 and receptor activator of nuclear factor kappaΒ ligand (RANKL) genes, and lung damage. Eighty-Five patients with COVID-19 were divided into two groups: mild and severe phases. The severe phase is defined as having a positive polymerase chain reaction (PCR) for SARS-CoV2, and acute pulmonary symptoms. The subjects' demographic, clinical, and paraclinical characteristics were collected according to a pre-prepared checklist. Total RNA was isolated from all samples using the Trizol kit to assess gene expression. The extracted product was then evaluated for the expression of miR-146a and the target genes (i.e., IL-18 and RANKL) using real-time PCR. The miR-146a gene's mean expression in mild and severe patients was 0.73 and 1.89, respectively, and this difference was statistically significant between the two groups. Also, the mean Expression of the IL-18 gene, 1.37±0.38 in the mild and 2.83±0.58 in the severe groups of the disease, demonstrated a significant difference between the two groups. In contrast, the expression levels of the RANKL gene did not show a significant difference between the two groups. Therefore, it may be hypothesized that altered levels of miR-146a may contribute to the severe COVID-19 that is more commonly observed in smokers, but further research is required. [ABSTRACT FROM AUTHOR]

Background: Familial Mediterranean fever (FMF) is common in Azari‐Turkish people, one of the biggest ethnic groups in Iran. In this study, we sought to investigate the mutation spectrum of the MEFV gene and any genotype–phenotype correlations. Methods and materials: 400 unrelated Azari‐Turkish FMF patients were analyzed in this study. Mutations in exons 2, 3, 5, and 10 of the MEFV gene were investigated using direct Sanger sequencing, and their correlations with the clinical features of the patients were analyzed. Results: At least one mutation was detected in 248 (62%) patients. The most common mutations were M694V (26.25%) and E148Q (24.75%), respectively. Abdominal pain (65.2%) and fever 204 (51%) were the most frequent clinical problems in all subjects. The analysis recognized a novel missense mutation in the coding region of the MEFV gene, named P313H, which is the first report of a new mutation in exon 2 of the MEFV gene in an Azari‐Turkish family. Conclusion: Genotype–phenotype correlations obtained from this study would be helpful in the diagnosis and management of FMF patients in clinical situations. This novel missense mutation may provide useful evidence for further studies of FMF pathogenesis. [ABSTRACT FROM AUTHOR]