肥胖风险因素促进新陈代谢重编程和病毒感染,在有1型高度炎症的气管中.
Paige Hartsoe1, Niccolette Schaunaman1, Taylor Nichols1
1Department of Medicine, National Jewish Health, Denver, CO 80206, USA.
Biomolecules
|September 27, 2025
概括
肥胖和1型炎症增加了犀牛病毒感染的风险. 抑制糖解路径可能会降低风险人群中的病毒严重程度.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢过程中的代谢.
- 病毒学 病毒学
背景情况:
- 肥胖与严重的呼吸道病毒感染有关,特别是在患有1型 (例如,干扰素- [IFN-γ]) 高炎症的喘患者中.
- 肥胖,和脂肪酸 (例如,棕酸[PA]) 和IFN-γ在呼吸道病毒感染中的相互作用仍然不清楚.
研究的目的:
- 在IFN-γ刺激下,研究高脂肪饮食 (HFD) 和PA在鼻病毒感染中的作用.
- 在与肥胖相关的病毒感染模型中探索糖解抑制剂的治疗潜力.
主要方法:
- 食HFD的小鼠模型被感染了犀牛病毒,并被IFN-γ刺激.
- 主要的人类气管支气管上皮细胞被用PA,IFN-γ和犀牛病毒治疗.
- 评估了2-脱氧-D-葡萄糖 (2-DG) 的作用,这是一种糖分解抑制剂.
主要成果:
- 在小鼠中,HFD和IFN-γ协同增加了肺鼻病毒水平和中性恋炎症.
- 在小鼠模型和人类呼吸道细胞中,PA和IFN-γ组合导致病毒载量升高.
- 通过HFD/PA和IFN-γ进行糖解的升级促进了病毒复制;2-DG治疗减少了病毒感染.
结论:
- 肥胖与1型高炎症相结合,增加了对严重呼吸道病毒感染的易感性.
- 向糖解路径或其代谢物提供了一个潜在的治疗策略,用于管理风险人群中的病毒感染.
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