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丙酮酸在甲型流感病毒感染期间影响巨噬细胞的炎症反应。

Pyruvate affects inflammatory responses of macrophages during influenza A virus infection.

机构信息

Department of Biology, Missouri State University, 901 S. National Ave. Springfield, MO, 65897, USA.

Department of Biology, Missouri State University, 901 S. National Ave. Springfield, MO, 65897, USA.

出版信息

Virus Res. 2020 Sep;286:198088. doi: 10.1016/j.virusres.2020.198088. Epub 2020 Jul 4.

DOI:10.1016/j.virusres.2020.198088
PMID:32634445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7345311/
Abstract

Pyruvate is the end product of glycolysis and transported into the mitochondria for use in the tricarboxylic acid (TCA) cycle. It is also a common additive in cell culture media. We discovered that inclusion of sodium pyruvate in culture media during infection of mouse bone marrow derived macrophages with influenza A virus impaired cytokine production (IL-6, IL-1β, and TNF-α). Sodium pyruvate did not inhibit viral RNA replication. Instead, the addition of sodium pyruvate alters cellular metabolism and diminished mitochondrial reactive oxygen species (ROS) production and lowered immune signaling. Overall, sodium pyruvate affects the immune response produced by macrophages but does not inhibit virus replication.

摘要

丙酮酸是糖酵解的终产物,被运入线粒体用于三羧酸 (TCA) 循环。它也是细胞培养基中的常用添加剂。我们发现,在流感 A 病毒感染小鼠骨髓来源的巨噬细胞时,培养基中添加丙酮酸会损害细胞因子的产生(IL-6、IL-1β 和 TNF-α)。丙酮酸钠并不抑制病毒 RNA 复制。相反,丙酮酸钠的添加改变了细胞代谢,减少了线粒体活性氧 (ROS) 的产生,并降低了免疫信号。总的来说,丙酮酸钠会影响巨噬细胞产生的免疫反应,但不会抑制病毒复制。

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