Chronic spontaneous urticaria (CSU) is a disorder characterized by recurrent transient itchy wheels of 6 weeks duration or longer. The cause cannot be pinpointed in about 40% of patients. To elucidate the possible association between CSU and hyperlipidemia, 40 CSU patients and 40 group matched healthy individuals were assessed for hyperlipidemia. Data on history, urticaria activity score (UAS-7), physical examination and routine laboratory investigations including (serum IL6 and TNF α) were recorded. Statistically significant increase of serum cholesterol, triglycerides (TG), low density lipoprotein (LDL), IL6, TNFα and decrease of high density lipoprotein (HDL) was found in CSU in comparison to control group. Regarding the different disease variables, both TG and cholesterol were positively correlated with duration of illness, urticaria score and TNF α. Serum LDL detected significant had a positive correlation with duration of illness, urticaria score, CRP and TNF α, while serum HDL detected had a significant negative correlation with TNF α. IL6 and TNFα associated systemic inflammation could be a common pathogenic mechanism of CSU and hyperlipidemia. Patients with CSU should be evaluated for hyperlipidemia.
Background: Natural-killer group 2 (NKG2), a characteristic receptor of natural killer (NK) cell family, assumes a vital role in modulating NK cytotoxic function. We aimed to detect mRNA expression of both NKG2A and NKG2D in serum NK cells obtained from colorectal cancer (CRC) patients. Methods: We enrolled 36 patients with newly diagnosed CRC, as well as 15 group matched healthy individuals. The patients were further classified into: 23 non-metastatic CRC (group 1) and 13 metastatic CRC (group 2). We detected the expression of NKG2A and NKG2D serum levels for all participants utilizing real-time polymerase chain reaction (RT-PCR). Results: NKG2D and NKG2A mRNA levels in peripheral blood mononuclear cells (PBMCs) were significantly elevated in patients with CRC compared to controls (P<0.01). NKG2D or NKG2A showed sensitivity (77.8, 83.33%) and specificity (73.33, 100%) respectively using receiver-operating characteristic (ROC) curve analysis for discrimination between patients and controls, whereas group 1 and group 2 showed no statistical significant difference in NKG2D and NKG2A levels (P>0.05). Conclusions: Our work is one of the first research that could detect an increase in NKG2D in CRC. In spite of their defensive role in tumor immune surveillance, NKG2D and NKG2A and their ligands could have misused as tumor survival tool, empowering immune avoidance and suppression.
Severity of symptoms in COVID-19 has been shown to result from a cytokine storm. Interleukin (IL)-17 is one of these various cytokines, which results in a proinflammatory response, systemic inflammatory symptoms, inflammatory cell infiltration of lung tissue and thus leads to the massive lung pathology and multiorgan failure. Gene polymorphisms in the regulatory regions of cytokine-encoding genes affect the amounts of cytokines produced and possess a fundamental role in infectious diseases. This study aimed to investigate the role of IL-17A (rs2275913; G197A) gene polymorphism as predictor of disease severity and its correlation with IL-17 serum levels in COVID-19 patients. A group of 70 COVID-19 patients and 17 age and sex-matched control subjects were enrolled in the present work. Patients were classified into two groups moderate, severe and acute respiratory distress (ARDS) cases, defined according to the criteria established by the world health organization. Quantitative real time-polymerase chain reaction was done to detect IL-17A (rs2275913; G197A). Serum IL-17 levels were assessed by an enzyme-linked immunosorbent assay in both patients and controls. The distribution of different IL-17A G/A genotypes among COVID-19 patients were 44.3% for GG genotype, 44.3% for AG genotype and 11.4% for AA genotype. Genotypes among the control group were 43.8% for GG genotype, 50% for AG genotype and 6.3% for AA genotype. G allele distribution was 66.4%, 68.8% in patient and control group, respectively, and A allele was 33.6% and 31.3%, respectively. There was no association between the different genotypes, disease severity or IL-17 serum levels in the patient group. In conclusion, despite the possible role of IL-17 in the pathogenesis of inflammation, there was no association between IL-17 polymorphism and disease severity or IL-17 serum levels among Egyptian COVID-19 patients.
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