Background: The etiopathogenesis of coronavirus disease 2019 (COVID-19) stem partially from the abnormal activation of the innate and adaptive immune systems. Here in the current investigation, the mRNA expression levels of toll-like receptors (TLRs) were evaluated in the nasopharyngeal epithelial cells from COVID-19 patients. Methods: Epithelial cells were obtained using nasopharyngeal swab samples from 90 COVID-19 patients and 50 controls. COVID-19 cases were classified into those without symptoms, with symptoms but not hospitalized, and with symptoms and hospitalized. To determine the mRNA expression levels of TLRs, first RNA was extracted and cDNA was synthesized, and finally Real-time PCR was exerted. Results: It was seen that the transcript levels of TLR3, TLR7, TLR8, and TLR9 were overexpressed in the COVID-19 patients with clinical symptoms needing hospitalization as well as in those with clinical symptoms without needing for hospitalization compared to controls. Upregulation of TLRs was associated with clinical presentations of the patients. Conclusions: Modulation of TLR3, TLR7, TLR8, TLR9 in the epithelial cells of COVID-19 cases may estimate the disease severity and requirement for hospitalization.

Previous studies have shown that several microRNAs (miRNAs) are dysregulated in the whole blood as well as diverse cells and tissues from rheumatoid arthritis (RA) patients. The aim of the current study was to determine if the expression of miR-146a, miR-103a, and miR-155 in whole blood of RA patients could confer potential markers in evaluating of activity-severity of the disease in RA patients with established disease. Whole blood samples were obtained from 30 RA patients and 30 healthy subjects. The RNA content of blood samples was isolated, cDNA was synthesized, and transcript levels of miR-146a, miR-103a, and miR-155 were determined using Real-time PCR. The clinicopathological characteristics of the patients were also evaluated. It was detected that expression level of miR-146a (fold change=1.85, P=0.004), miR-103a (fold change=2.44, P=0.0018), and miR-155 (fold change=1.94, P=0.0025) were significantly upregulated in the whole blood samples of RA patients in comparison to that of healthy subjects. Expression level of miRNAs was correlated with clinicopathological characteristics of the patients, including Disease Activity Score 28 (DAS28), Simple Disease Activity Index (SDAI), 28Tender Joint Count (TJC-28), 28Swollen Joint Count (SJC-28), C-reactive protein (CRP), Rheumatoid factor (RF), and anti-cyclic citrullinated peptide (anti-CCP) antibodies. Upregulated levels of miR-146a, miR-103a, and miR-155 in the whole blood samples of RA patients could confer a potential marker of activity-severity of the disease in RA patients with established disease.

Promoting prevalence of metabolic syndrome (MetS) in Rheumatoid arthritis (RA) patients might occur secondary to RA therapy as well as sedentary life style. However, conflicting observations have been reported on the correlation between MetS and RA. This study aimed to determine the frequency of MetS and association of its components in RA. In this study, 500 RA patients and 500 age- and gender-matched healthy controls were enrolled. MetS was fulfilled through the International Diabetes Federation (IDF) criteria. A multivariate regression model was used to control for variables independently associated with the risk of MetS in RA patients. The prevalence of MetS was 58.8% on IDF criteria in RA patients that was higher than controls (20.4%). Higher incidence of cardiovascular disease (CVD), the familial history of CVD, hypertension, type 2 diabetes mellitus (T2DM), smoking, dyslipidemia, and higher levels of body mass index (BMI), waist circumference (WC), total cholesterol level, fasting blood sugar (FBS), triglyceride (TG) level, low-density lipoprotein (LDL) level, while lower levels of high-density lipoprotein (HDL) were associated with an increased risk of MetS in RA patients. Multivariate regression analysis indicated that age, WC, dyslipidemia, LDL, and DAS28 were independent predictors of MetS in the RA patients. The prevalence of MetS is higher in RA patients. Our findings suggest an association between cardiovascular risk factors and the increased prevalence of MetS in RA patients.

Background: Interleukin-17 (IL-17) family plays a role in the pathogenesis of knee osteoarthritis (KOA) by contributing to the inflammatory and destructive processes in the affected joint. This study aimed to measure levels of IL-17 A and IL-25 (IL-17E) in serum of KOA patients and determine their roles in the disease severity of patients. Methods: In this, 34 patients with KOA and 30 age and sex-matched healthy subjects (HS) were enrolled. Patients were categorized based on their Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), Visual Analog Scale (VAS), and Body Mass Index (BMI) scores. The enzyme-linked immunosorbent assay (ELISA) technique was employed to measure serum levels of IL-17 A and IL-25. Results: Level of IL-25 was significantly higher (P < 0.0001) in the KOA subjects than HS. IL-17 A level was significantly higher in KOA cases with WOMAC < 40 (P < 0.0001) in comparison to HS. IL-25 level was significantly higher in the KOA cases with WOMAC < 40 (P < 0.0001) and with WOMAC ≥ 40 (P < 0.0001) compared to HS. IL-17 A concentration was significantly higher in the KOA cases with VAS < 5 (P < 0.0001) compared to HS. IL-25 level was significantly higher in the KOA cases with VAS < 5 (P < 0.0001) and with VAS ≥ 5 (P < 0.0001) in comparison to HS. KOA patients with BMI ≥ 30 had significantly higher IL-17 A and IL-25 concentration in comparison to HS. Conclusions: The serum level of IL-25 in KOA patients is increased probably due to negative controlling feedback on inflammatory responses, which can be associated with obesity and disease activity.

Background: Peptidyl arginine deiminase 4 (PADI4) has been implicated in Rheumatoid arthritis (RA) pathogenesis. Here we aimed to evaluate the association of PADI4 gene rs11203367 and rs1748033 single nucleotide polymorphisms (SNPs) with RA proneness. Methods: The mRNA expression of PADI4 was determined in the whole blood samples. The genotyping of PADI4 polymorphisms was conducted using allelic discrimination TaqMan genotyping Real-time PCR. Results: The alleles and genotypes of rs11203367 polymorphism were not associated with susceptibility to RA risk. The T allele (OR = 1.58, 95%CI: 1.21–2.04, P = 0.0005), TT genotype (OR = 2.79, 95%CI: 1.53–5.06, P = 0.0007), TC genotype (OR = 1.52, 95%CI: 1.04–2.23, P = 0.0291), dominant (OR = 1.72, 95%CI: 1.19–2.47, P = 0.0034) and recessive (OR = 2.19, 95%CI: 1.25–3.82, P = 0.0057) models of rs1748033 SNP were associated with higher risk of RA. There was a significant upregulation of PADI4 mRNA in the RA patients compared to controls. mRNA expression of PADI4 had significantly positive correlation with anti-CCP level (r = 0.37, P = 0.041), RF level (r = 0.39, P = 0.037), and CRP level (r = 0.39, P = 0.024). Conclusion: PADI4 gene rs1748033 SNP was associated with increased RA risk. This polymorphism might affect the RA pathogenesis regardless of impressing the levels of PADI-4 in serum.