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1.
Turkish Journal of Biochemistry ; 46(SUPPL 2):29, 2021.
Article in English | EMBASE | ID: covidwho-1770803

ABSTRACT

BACKGROUND AND AIM: COVID-19, caused by a new coronavirus, SARSCoV2, which emerged in the animal market in Wuhan, China in December 2019, causes severe acute respiratory syndrome. The coronavirus is structurally 2 single-chain, positive polarity, enveloped, ribonucleic acid viruses. It targets the respiratory system. In clinical studies, it has been found to cause a cytokine storm that leads to multi-organ failure. Cytokines are small molecular weight, soluble proteins released by immune cells. The most important is Interleukin-1 β (IL-1β). In this study, it was aimed to determine the levels of IL-1β, which is secreted from innate immune system cells such as monocytes, macrophages and dendritic cells, in patients with COVID-19. METHODS: COVID-19 positive patients (n=52) and healthy individuals without any systemic disease (n=35) were included in the study. IL-1β levels from serum samples of patient and control groups were studied by ELISA method in DSXTM Four-Plate Automated ELISA Processing System microELISA device. Statistical analyzes were performed with SPSS Statistic (IBM Corporation, Somers, NY) software version 17. Data were given as median [25P-75P] with the Mann- Whitney U Test. RESULTS: IL-1β levels were 892.09 mg/dL in the patient group;[821.88- 1189.01], while 828.55 mg/dL in the control group;[720,70-1387,55]. Although IL-1β levels increased in the patient group compared to the control group, there was no statistically significant difference (p>0.211). CONCLUSIONS: CONCLUSION: By using the data of the study, further studies are recommended to show the effects of IL-1 BETA level on COVID-19 positive patients.

2.
Turkish Journal of Biochemistry ; 46(SUPPL 2):36, 2021.
Article in English | EMBASE | ID: covidwho-1766624

ABSTRACT

BACKGROUND AND AIM: The source of COVID-19, which was declared a pandemic in March 2020, is coronavirus called Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Our immune system to eliminate infectious agents such as SARS-COV-2;It uses cellular elements such as lymphocytes, monocytes/macrophages, neutrophils, dendritic cells, NK cells and platelets, dissolved molecules such as cytokines, chemokines, acute phase proteins and complements that work in harmony with each other. Cytokines are regulatory proteins. They undertake tasks such as proliferation, differentiation and activation of cellular elements such as leukocytes. In this study, it was aimed to investigate relationship between cytokines and immunophenotypic characters of leukocyte subgroups in COVID-19 patients. METHODS: In this study, 51 COVID-19 patients (18-71 years) were included who outpatient applied to Mersin University Hospital and were positive for COVID-19 according to PCR (Bio-Speedy RT-qPCR Detection Kit, Bioeksen, Turkey) analysis. Samples taken on the application day were included in the study. Immunophenotype analyzes were measured by flow cytometry using the FACSCalibur (Becton Dickinson, USA) instrument. Cytokine levels (IL-1β and IL-6) were studied with the ELISA method (DSX-4-Plate Automated, Dynex, USA). RESULTS: Correlations of cytokines and leukocyte subgroups were examined, respectively, in CD3+ T-lymphocytes (r=-0,034-r=-0,096), CD4+ T-Helper (r=-0,035-r=-0,074), CD8+ T-cytotoxic (r=0,097-r=0,135), CD19+ B-lymphocytes (r=0,020-r=0,09), HLA-DR+ lymphocytes (r=0,064-r=0,006), CD56+ NK cells (r=-0,023-r=0,57). No correlation was observed between IL-1β and IL-6 and leukocyte subgroups (P>0.05). A strong positive correlation was found between IL-1β and IL-6 (r=0.894, p<0.05). CONCLUSIONS: New approaches are needed in the treatment of COVID-19 patients, especially in patients with cytokine storm. Due to do there was no significant correlation between IL-1β and IL-6 and the immunophenotypic characters of leukocyte subgroups, and a strong positive correlation was observed between IL-1β and IL-6, it was thought that monitoring proinflammatory cytokines in patients would be of clinical benefit.

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