Infection with influenza A (H1N1) virus contributes significantly to the global burden of acute respiratory diseases. Glucose uptake and metabolic changes are reported in different cell types after infections with different virus types, including influenza A virus. Alteration of glucose metabolism specifically in immune cells has major health consequences. The aim of this study was to monitor glucose concentration in unstimulated and stimulated U937 human monocytes with infectious or heat inactivated H1N1 or Staphylococcus aureus or in nonpathogenically stimulated monocytes with phorbol-12-myristate-13-acetate. Stimulated or unstimulated U937 human monocytes were subjected to H1N1 infection for different time points and the glucose profile in the growth medium was measured post infection. Results showed that regardless to whether the initial stimuli on U937 cells were of pathogen or nonpathogen origins, challenge infection by H1N1 causes a significant reduction of glucose levels 36 h post infection. In conclusion, H1N1 infection has a direct effect on the glucose uptake of U937 cells in vitro. This effect can be related to either H1N1 infection or cell differentiation status that might occur due to the exerted stimuli.

中文翻译：

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H1N1感染会降低人U937单核细胞培养物中的葡萄糖水平。

甲型流感（H1N1）病毒感染对急性呼吸道疾病的全球负担做出了重大贡献。据报道，不同类型的病毒（包括甲型流感病毒）感染后，不同细胞类型的葡萄糖摄取和代谢变化。特别是免疫细胞中葡萄糖代谢的改变对健康有重大影响。这项研究的目的是监测感染或热灭活的H1N1或金黄色葡萄球菌在未刺激和刺激的U937人单核细胞中的葡萄糖浓度或用佛波12-肉豆蔻酸13-醋酸酯非病原性刺激的单核细胞。将受刺激或未受刺激的U937人单核细胞在不同时间点进行H1N1感染，并在感染后测量生长培养基中的葡萄糖谱。结果表明，无论U937细胞最初的刺激是病原体还是非病原体来源，H1N1激发感染均可在感染后36小时显着降低葡萄糖水平。总之，H1N1感染对U937细胞的葡萄糖摄取的直接作用在体外。此作用可能与H1N1感染或由于施加刺激而可能发生的细胞分化状态有关。