Role of microRNA-16-5p, microRNA-194, IP-10 and APRIL in inducing inflammation in SARS-CoV-2 infected patients with severe symptoms

INDIAN JOURNAL OF EXPERIMENTAL BIOLOGY(2023)

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摘要
The immune system induces pro-inflammatory conditions in the hospitalized SARS-CoV-2 infected patients. The roles played by humoral immunity-related factors in the pro-inflammatory conditions of the patients are yet to be clarified. It has been revealed that a proliferation-inducing ligand (APRIL), interferon (IFN)-gamma-inducible protein 10 (IP-10) and microRNA-16-5p (miR-16-5p) play key roles in the induction of inflammation. Thus, in this study, we explored the expression levels of APRIL, IP-10, miR16-5p and miR-194 in the SARS-CoV-2 infected patients with severe symptoms. In addition, miR-194 can inhibit immune responses against viral infection. Further, we evaluated the expression of the molecule in the patients to explore the effect of the molecule during coronavirus disease 2019 (COVID-19). About 60 severe SARS-CoV-2 infected patients who were in the peak of the disease and 60 healthy controls were enrolled to evaluate APRIL, IP-10, miR16-5p and miR-194 expression levels. IP-10 expressions were evaluated using enzyme linked immunoassay (ELISA), while APRIL, miR-16-5p and miR-194 were evaluated using Real-Time PCR technique. The results showed that APRIL, miR-16-5p and miR-194 expression and serum levels of IP-10 significantly increased in the hospitalized SARS-CoV-2 infected patients compared to the healthy controls. There was a positive correlation between miR-16-5p and miR-194 expression levels in the patients. The significant participation of miR-16-5p in the induction of inflammation indicates its key role along with APRIL and IP-10 for excess inflammation in the hospitalized SARS-CoV-2 infected patients with severe symptoms. Upregulation of miR-194 may be natural negative feedback to the pro-inflammatory conditions and may be associated with establishment of SARS-CoV-2 infection.
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关键词
COVID-19,Humoral immunity,differentiation (CD) 40L-independent antibody
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