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• W4378965467 abstract "Abstract Background Delayed diagnosis and inadequate treatment caused by limited biomarkers were associated with outcomes of COVID-19 patients. It is necessary to find other promising biomarkers and candidate targets for defining dysregulated inflammatory state besides the typical biomarkers and drug targets have been used clinically. Methods In a cohort of hospitalized COVID-19 patients with varying degrees of illness severity, we characterized TREM-1 and TREM-2 expression in plasma and on the surface of cell subpopulations using ELISA and flow cytometry, respectively. And their correlations with disease severity and contrast with main clinical indicators were evaluated. Results We found the increased expression of soluble TREM-1 and TREM-2 in plasma from COVID-19 patients compared to the control group. Moreover, membrane-bound TREM-1 and TREM-2 expression was also upregulated on the cell surface of circulating blood T cells from COVID-19 patients. Correlation analysis results showed the sTREM-2 level was negatively correlated with PaO2/FiO2, but positively correlated with CRP, PCT and IL-6 level. Receiver operating characteristic (ROC) curves presented that TREM-1 and TREM-2 exhibited strong predictive abilities, and their expression was equal to CRP and IL-6, and better than leukocytes or neutrophil absolute count and PCT in distinguishing disease severity. Conclusion These results highlighted the important role of TREM-1 and TREM-2 in viral infection. TREM-2 and TREM-1 were critical host immune factors in response to SARS-COV-2 infection and could serve as potential diagnostic and therapeutic biomarkers of COVID-19." @default.
• W4378965467 created "2023-06-02" @default.
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• W4378965467 date "2023-05-30" @default.
• W4378965467 modified "2023-10-15" @default.
• W4378965467 title "TREM-1, TREM-2 and their association with disease severity in patients with COVID-19" @default.
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• W4378965467 doi "https://doi.org/10.21203/rs.3.rs-2986092/v1" @default.
• W4378965467 hasPublicationYear "2023" @default.
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