Aims This study aimed to make a comparison between the clinical laboratory-related factors, complete blood count (CBC) indices, cytokines, and lymphocyte subsets in order to distinguish severe coronavirus disease 2019 (COVID-19) cases from the non-severe ones. Materials and methods Relevant studies were searched in PubMed, Embase, Scopus, and Web of Science databases until March 31, 2020. Cochrane's Q test and the I 2 statistic were used to determine heterogeneity. We used the random-effect models to pool the weighted mean differences (WMDs) and 95% confidence intervals (CIs). Key findings Out of a total of 8557 initial records, 44 articles (50 studies) with 7865 patients (ranging from 13 to 1582), were included. Our meta-analyses with random-effect models showed a significant decrease in lymphocytes, monocyte, CD4+ T cells, CD8+ T cells, CD3 cells, CD19 cells, and natural killer (NK) cells and an increase in the white blood cell (WBC), neutrophils, neutrophil to lymphocyte ratio (NLR), C-reactive protein (CRP)/hs-CRP, erythrocyte sedimentation rate (ESR), ferritin, procalcitonin (PCT), and serum amyloid A (SAA), interleukin-2 (IL-2), IL-2R, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor-alpha (TNF-α), and interferon-gamma (INF-γ) in the severe group compared to the non-severe group. However, no significant differences were found in IL-1β, IL-17, and CD4/CD8 T cell ratio between the two groups. Significance Decrease in total lymphocytes and lymphocyte subsets as well as the elevation of CRP, ESR, SAA, PCT, ferritin, and cytokines, but not IL-1β and IL-17, were closely associated with COVID-19 severity, implying reliable indicators of severe COVID-19.

This study aims to evaluate the effects of treatment with IFN-β 1α on the expressions of NLRP3, NLRP1, NLRC4, and AIM2, as inflammasomes, and caspase-1, IL-1β, and IL-18, as the downstream molecules of inflammasomes, in a population of Iranian multiple sclerosis (MS) patients. In this study, 30 MS patients (22 women and 8 men) participated. Before receiving any medication and 6 months after treatment with standard doses of IFN-β 1α 30 mcg injected intramuscularly once a week, blood samples were taken and then the leukocytes isolated, total RNAs extracted, and complementary DNAs (cDNAs) synthesized. Gene expressions of NLRP3, NLRP1, NLRC4, AIM2, and ASC were evaluated at messenger RNA (mRNA) levels using real-time PCR method; for assessing caspase-1 at protein level, the Western blot method was used. The amounts of IL-1β and IL-18 were measured in plasma using enzyme-linked immunosorbent assay method. Analysis of the results before and after therapy with IFN-β 1α in all patients shows significantly decreased expressions of NLRP3, NLRC4, and AIM2. The plasma levels of IL-1β, after treatment with IFN-β 1α, were significantly decreased in the MS patients. Based on our results, it appears that NLRP3, NLRC4, and AIM2 play critical roles in the progression of MS, probably by mediating Th1 and Th17 responses. It seems that decreased expression of IL-1β is related to decreased production and also functions of inflammasomes.

Objective Curcumin is the well-known compound which is extracted from turmeric powder, the dried rhizome of the Curcuma longa Linn. This have been used for the treatment of various disorders including inflammation. In this study we have analyzed the effect of curcumin on arthritis induced by adjuvant in rats, considering changes in methionine sulfoxide reductase A (MSRA) expression and antioxidant enzymes levels. Methods Five groups of adult male Wistar rats (n=10), were randomly selected as control, placebo, experimental 1, 2 and 3. The induction of arthritis was carried out by injection of 0.1 ml adjuvant in plantar region. The first experimental group received no curcumin treatment, whereas the experimental two and three received curcumin (1 and 2 g/kg daily) respectively, for fourteen days. MSRA gene expression was assessed by real-time PCR and protein levels of MSRA, SOD, CAT and GPx were analyzed via ELISA method. Results The results showed no significant weight changes among the groups during the experimental period and the paw swelling caused by adjuvant was recovered within fourteen days of treatment with curcumin. However, the levels of enzymes such as superoxide dismutase, catalase and glutathione peroxidase were increased by a dose dependent manner. These results also illustrated that the gene expression and protein level of MSRA in groups treated with curcumin increased significantly ( p ≤0.05). Conclusion We concluded that the curcumin can be used against inflammation. The increasing level of MSRA can be due to the antioxidant effect of curcumin. The enzymatic level changes (MSRA, SOD, CAT and GPx) may interfere with the aging process and delay it.

Objectives: Interferon-β 1a (IFN-β 1a) is a common strategy therapy for multiple sclerosis (MS) with unknown mechanisms. S100A12 (S100 calcium-binding protein A12) is a damage-associated molecular pattern molecule which binds to its receptor, RAGE (receptor for advanced glycation end products), and activates nuclear factor-κB (NF-κB). NF-κB is transcribed from proinflammatory molecules, which may participate in the pathogenesis of MS. Therefore, the aims of this study were to compare mRNA levels of S100A12, RAGE, and NF-κB in newly diagnosed MS patients with healthy controls and determine whether IFN-β 1a therapy affects the expression of the molecules. Methods: S100A12, RAGE, and NF-κB mRNA levels in 30 new cases of untreated MS patients and 35 healthy controls were evaluated using the real-time PCR technique. The mRNA levels were also evaluated in the MS patients after 6 months of IFN-β 1a therapy. Results: S100A12, RAGE, and NF-κB mRNA levels were significantly decreased in the new cases of untreated MS patients in comparison to healthy controls. IFN-β 1a therapy results in upregulation of RAGE in MS patients, but not S100A12 and NF-κB. Conclusions: It appears that S100A12 participates in the pathogenesis of MS, and it seems that IFN-β 1a modulates immune responses in an S100A12-independent manner. Based on the reported anti-inflammatory effects of RAGE, it seems that RAGE may be considered as a mechanism by IFN-β 1a to modulate immune responses. NF-κB is produced permanently in the human cells and is inactive in the cytoplasm; therefore, the effects of IFN-β 1a may be related to its functions rather than expressions.

The aims of this study were to compare mRNA levels of melanoma differentiation‐associated protein 5 (MDA5) and retinoic acid‐inducible gene 1 (RIG‐1) in multiple sclerosis (MS) patients in comparison to the healthy controls as well as investigating the effects of IFN‐β 1a on the expression of these molecules. In this study, mRNA levels of MDA5 and RIG‐1 in peripheral leukocytes of 30 new cases of MS patients and 35 healthy controls were evaluated using the real‐time‐PCR method. mRNA levels of MDA5 and RIG‐1 were determined in the MS patients 6 months after treatment with standard doses of IFN‐β 1a. mRNA levels of MDA5 and RIG‐1 were significantly decreased in the MS patients in comparison to the healthy controls. The analysis also revealed that IFN‐β 1a therapy leads to the upregulation of RIG‐1, but not MDA5, in the total MS patients and the female group. MS patients suffer from insufficient expression of MDA5 and RIG‐1, and IFN‐β 1a therapy results in the upregulation of RIG‐1 in the patients, especially in the female patients. Thus, it seems that IFN‐β 1a not only decreased pathogenic inflammatory responses but also modulated the expression of RIG‐1 to protect the patients from infectious diseases and upregulation of IFN‐I in a positive feedback.