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老年小鼠烧伤后的存活情况及细胞介导免疫

Survival and cell mediated immunity after burn injury in aged mice.

作者信息

Kovacs Elizabeth J, Grabowski Kristy A, Duffner Lisa A, Plackett Timothy P, Gregory Meredith S

机构信息

Immunology and Aging Program, Loyola University Chicago, Maywood, IL ; Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago, Stritch School of Medicine, Building 110, Room 4221, 2160 South First Avenue, Maywood, IL 60153 ; Burn and Shock Trauma Institute, Loyola University Chicago, Maywood, IL ; Department of Surgery, Loyola University Chicago, Stritch School of Medicine, Building 110, Room 4221, 2160 South First Avenue, Maywood, IL 60153.

出版信息

J Am Aging Assoc. 2002 Jan;25(1):3-9. doi: 10.1007/s11357-002-0001-4.

Abstract

The elderly are less able to survive burn injury than young healthy individuals. Regardless of age, burn victims often succumb to secondary infections rather than the primary injury. Since immune responses diminish with age, it is likely that aged individuals are predisposed to a poor outcome by virtue of their weak immune system. Elevated production of macrophage-derived mediators, including interleukin-6 (IL-6), may lead to post-injury immunosuppression in young adults. Healthy aged individuals produce high circulating levels of these mediators; therefore, the combination of the age and burn trauma could further suppress immune responses and contribute to the rapid demise of aged burn patients. Herein, the effects of age and burn trauma using a murine scald injury model were examined. After injury, aged mice are less likely to survive, are unable to mount immune responses, and produce more IL-6 when compared to young adult mice given the same size injuries. Enhancing our understanding of the mechanisms responsible for regulating cell-mediated immune responses after injury could lead to the development of therapies designed to treat aged burn patients.

摘要

老年人比年轻健康个体更难以在烧伤后存活。无论年龄大小,烧伤患者往往死于继发性感染而非原发性损伤。由于免疫反应会随着年龄增长而减弱,老年人很可能因其免疫系统薄弱而易于出现不良后果。包括白细胞介素-6(IL-6)在内的巨噬细胞衍生介质的产生增加,可能导致年轻成年人受伤后免疫抑制。健康的老年人会产生高循环水平的这些介质;因此,年龄和烧伤创伤的共同作用可能会进一步抑制免疫反应,并促使老年烧伤患者迅速死亡。在此,我们使用小鼠烫伤模型研究了年龄和烧伤创伤的影响。受伤后,与遭受相同程度损伤的年轻成年小鼠相比,老年小鼠存活的可能性更小,无法产生免疫反应,并且会产生更多的IL-6。加深我们对损伤后调节细胞介导免疫反应机制的理解,可能会促使开发出针对老年烧伤患者的治疗方法。

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