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Published on: March 9, 2022
Dynamic Changes of Plasma Mitochondrial DNA in Neonates with Acute Respiratory Distress Syndrome
Xiaoping Fan1, Jiang Junsheng1
1Department of Pediatrics, Linping Branch, The Second Affiliated Hospital of Zhejiang University, Hangzhou, China.
Abstract:
Background: This study aimed to analyze mitochondrial DNA levels in neonates with neonatal acute respiratory distress syndrome(ARDS). Method: Neonates diagnosed with ARDS from January 2021 to January 2023 were prospectively included as a study group. The control group was selected from healthy neonates during the same period. Real-time quantitative PCR was used to quantity plasma mtDNA levels. Peripheral blood mononuclear cells were isolated, and the expression levels of cGAS and STING mRNA were measured by real-time quantitative PCR. Peripheral blood mononuclear cells were co-cultured with mtDNA, and ELISA was used to determine the levels of serum IL-6, IL-23, and IFN-γ. Pearson correlation analysis was used to assess the correlation between serum mtDNA and serum IL-6, IL-23, and IFN-γ levels. Results: this study included 25 with mild ARDS, 15 with moderate ARDS, and 10 with severe ARDS, alongside 25 neonates in healthy control group. Compared with the control group, plasma mtDNA levels, serum levels cGAS-STING mRNA, IL-6, IL-23, and IFN-γ were significantly increased in the ARDS groups (p < 0.05). Compared with the mild ARDS group, plasma mtDNA, serum cGAS-STING mRNA, IL-6, IL-23, and IFN-γ levels were significantly increased in the moderate and severe ARDS groups (p < 0.05). Furthermore, compared with day 1, plasma mtDNA, serum cGAS-STING mRNA, IL-6, IL-23, and IFN-γ levels significantly increased on day 3 and significantly decreased on day 7 in all ARDS groups (p < 0.05). Pearson correlation analysis showed that mtDNA levels were correlated with serum IL-6, IL-23, IFN-γ, and cGAS-STING mRNA levels (p < 0.05). Conclusion: Our data demonstrate a potential role of mtDNA with ARDS patients, which may produce inflammatory mediators by activating the cGAS/STING signaling pathway.
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