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衰老、炎症失衡和病毒感染。

Aging, imbalanced inflammation and viral infection.

机构信息

Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.

出版信息

Virulence. 2010 Jul-Aug;1(4):295-8. doi: 10.4161/viru.1.4.12009.

Abstract

Older people experience enhanced susceptibility to viral infections and subsequent superimposed bacterial infections. Based on both experimental and clinical studies, this susceptibility is thought to be due to declining immune responses. However, our work indicates that older people may succumb to viral infection due to exaggerated immune responses as aged mice produce higher serum levels of the inflammatory mediator IL-17 than younger mice upon herpes viral infection. These age-elevated IL-17 responses induce a lethal immune pathology during viral infection. Early during the course of infection natural killer T-cells (NKT-cells) are major contributors to the elevated IL-17 response in aged mice. These responses synergize with defective viral clearance with aging noted by impaired IFN-α responses by plasmacytoid DCs. Our results indicate that novel anti-inflammatory drugs may resolve imbalanced inflammation and improve outcomes in older people infected with viruses.

摘要

老年人更容易受到病毒感染,并随后发生继发细菌感染。基于实验和临床研究,这种易感性被认为是由于免疫反应下降所致。然而,我们的工作表明,老年人可能由于过度的免疫反应而感染病毒,因为在疱疹病毒感染后,老年小鼠比年轻小鼠产生更高水平的炎症介质白细胞介素-17。在病毒感染期间,这些年龄增加的白细胞介素-17 反应会引起致命的免疫病理。在感染早期,自然杀伤 T 细胞(NKT 细胞)是老年小鼠中白细胞介素-17 反应升高的主要贡献者。这些反应与衰老时的病毒清除缺陷协同作用,表现为浆细胞样树突状细胞的 IFN-α 反应受损。我们的研究结果表明,新型抗炎药物可能缓解失衡的炎症反应,并改善老年人感染病毒后的结局。

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