PATIENTS AND METHODS: Materials and Methods: The systematization of literature data on the role of cytokines in the progression of HF in patients with concomitant thyroid pathology (TP) was carried out. The results of our own research were presented.
CONCLUSION: Conclusions: The final chapter in the history of the role of cytokines in the progression of HF has not yet been written. Further studies, including genetic ones, are necessary. The patients with HF have higher levels of TNFβ and IL-6, and a lower concentration of IL-4, compared to the control group. Patients with a fatal outcome of the disease, in contrast to those who survived for two years, have an increased level of TNFβ. In patients with concomitant TP, who had repeated hospitalization, a lower level was registered, compared to that under conditions of a more favorable course of heart failure. Concentrations of cytokines in the blood of patients with HF are associated with gene polymorphisms of the β-adrenoreceptor system: the C-allele of the Gly389A polymorphism of the β1-adrenoceptor gene leads to a decrease in the risk of increasing TNFα; IL-1α increases in the presence of the A-allele of the Ser49Gly polymorphism of this gene. In patients with HF and concomitant thyroid pathology, the risk of IL-6 growth increases in homozygous (C) patients for the Ser275 polymorphism of the β3 subunit of the G-protein.
METHODS: Microscopic agglutination test (MAT)-positive and MAT-negative human serum samples (n=30) from patients with leptospirosis were obtained from the Public Health Laboratory, Kota Kinabalu, Sabah, Malaysia and control serum samples (n=10) were obtained from healthy student volunteers. We estimated the levels of IL-1β, IL-6, IL-8, IL-10, and TNF-α in serum samples by a Luminex assay.
RESULTS: The levels of IL-6, IL-8, and IL1-β were significantly higher in 13% of the patients with leptospirosis compared to the healthy controls, while the levels of IL-10 and TNF-α were not elevated in either group.
CONCLUSION: Our data suggest that elevated levels of IL-6, IL- 8, and IL1-β may be associated with leptospirosis disease severity, which requires patient follow-up for confirmation.
AIM: The purpose of this study was to investigate the relationship between -174 G>C IL-6 polymorphism gene on the level of IL-6 and CRP in the population of western Indonesia obese who are obese.
METHODS: In this study, we examined 178 subjects consisting of 89 who are obese with BMI> 25, and controls with BMI between 18.5 and 23. Fasting blood was taken from each subject for the examination of IL-6 and CRP levels by the ELISA method. Determination of genotype -174 G>C IL-6 gene was examined by Polymerase Chain reaction- Restriction Fragment Length Polymorphism (PCR-RFLP) methods.
RESULTS: The results of this study showed increased levels of IL-6 and CRP in the obese group compared to the controls. In the obese group, CC genotype had higher CRP and lower IL-6 levels than the GC and GG genotypes. The frequency of CC genotype in the obese group was 47.2% compared with 28.1% in controls and this genotype was considered a risk factor for obesity. Carriers of the C genotype as a dominant or a recessive model had greater risk of obesity.
CONCLUSION: It was concluded that the polymorphism - 174G>C IL-6 gene is a risk factor for obesity and is associated with increased levels of IL-6 and CRP in an obese group of the Western Indonesian ethnic population.
MATERIALS AND METHODS: A total of 24 male rats were randomly divided into six groups: control, DM 1.5 month (DM1.5), DM 2 months (DM2) and the group with three different doses of CGA 12.5 (CGA1), 25 (CGA2), and 50 (CGA3) mg/KgBW. Frontal lobe tissue is taken for analysis of mRNA expression for NF-κB, MCP-1, IL-6, and GFAP using Reverse Transcriptase PCR (RT-PCR). Samples were also taken for histopathology preparation and stained by immunohistochemistry method using anti-GFAP antibodies to observe glial cell activation in frontal lobe tissue.
RESULTS: The group that was given CGA at all doses have statistically significant better memory function, i.e. DM2 versus CGA1 (p = 0.036), CGA2 (p = 0.040), and CGA3 (p = 0.021). The result of mRNA expression in NF-κB was lower in the group given CGA, i.e. DM2 compared to CGA2 (p = 0.007). mRNA expression of MCP-1 was significantly lower in all CGA treatment groups compared to the non-CGA group (p = 0.000). IL-6 mRNA expression was lower than the group not given CGA, DM compared to CGA2 (p = 0.028). GFAP mRNA expression was lower than the group given CGA in DM, DM2 group compared to CGA1 (p = 0.04) and CGA3 (p = 0.004).
CONCLUSION: Administration of CGA can improve memory function at all doses given, and can reduce brain inflammatory activity, especially in the CGA2 group.
MATERIALS AND METHODS: Thirty-nine formalin-fixed paraffin-embedded ameloblastoma cases comprising unicystic ameloblastoma (n=19) and solid/multicystic ameloblastoma (n=20) were subjected to IHC staining for IL-1α, IL-1β, IL-6 and IL-8. A semi-quantitative method was used to evaluate the expression levels of these cytokines according to cell types in the tumoural parenchyma and stroma.
RESULTS: Major findings were upregulations of IL-1α and IL-6 in SMA compared to UA. Both cytokines were heterogeneously detected in the tumoural parenchyma and stroma. Within the neoplastic epithelial compartment, IL-1α expression was more frequently detected in PA-like cells in UA whereas it was more frequently encountered in SR-like cells in SMA. IL-6 demonstrated higher expression levels in the stromal compartment of SMA. IL-1β and IL-8 were markedly underexpressed in both tumour subsets.
CONCLUSIONS: Overexpression of IL-1α in SMA suggests that this growth factor might play a role in promoting bone resorption and local invasiveness in this subtype. The expression levels of IL-1α and IL-6 in three cellular localizations indicate that parenchymal-stromal components of ameloblastoma interact reciprocally via IL-1α and IL-6 to create a microenvironment conducive for tumour progression.
MATERIALS AND METHODS: A total of 42 OA patients diagnosed with OA and treated in our hospital from January 2017 to January 2018 were selected as the subjects, and 28 healthy people were enrolled as controls. The expressions of interleukin-1 beta (IL-1β) and IL-6 in the plasma of OA patients were detected via immunohistochemical staining. Moreover, the knee joint function of OA patients was evaluated by Lysholm score, Western Ontario and McMaster Universities (WOMAC) score and Visual Analogue Scale (VAS) score. The expression levels of plasma miR-146a and miR-365 in OA patients were measured through RT-PCR. Besides, the significance of the expression levels of miR-146a and miR-365 for the diagnosis of OA was analysed by ROC curves.
RESULTS: As compared with healthy people, OA patients had elevated expression levels of plasma IL-1β and IL-6, decreased Lysholm score, increased WOMAC and VAS scores as well as significantly up-regulated levels of plasma miR-146a and miR-365, which were of important significance for diagnosis.
CONCLUSION: The expression levels of plasma miR-146a, miR-365 and inflammatory factors are notably higher, the disease is more severe, and the function of knee joint movement is weaker in OA patients than those in healthy controls. It can be concluded that the levels of both miR-146a and miR-365 can serve as biomarkers of OA diagnosis.
Methods: A total of 80 NT and 80 PreHT healthy subjects aged between 18-45 years were recruited in Kuantan, Pahang, Malaysia using an observational cross-sectional study approach. DNA methylation level of IL-6 promoter in peripheral leukocytes were measured using bisulphite conversion and MethyLight assay.
Results: There was no significant difference in age between NT and PreHT (P = 0.655). The mean blood pressure was 110(8)/73(5) mmHg in NT and 125(7)/82(5) mmHg in PreHT subjects. The IL-6 promoter methylation level was significantly lower in PreHT compared to NT subjects (P < 0.001).
Conclusion: The current study demonstrates that hypomethylation of IL-6 promoter was associated with pre-hypertension in young adults. Thus, IL-6 methylation could be used as an early indicator for predicting hypertension and related risk of cardiovascular diseases in prehypertensive subjects. Gene expression and longitudinal studies are warranted to examine the methylation effect on IL-6 expression over time.