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老年患者脓毒症的免疫发病机制。

The immunopathogenesis of sepsis in elderly patients.

作者信息

Opal Steven M, Girard Timothy D, Ely E Wesley

机构信息

Infectious Disease Division, Brown University School of Medicine, Providence, Rhode Island, USA.

出版信息

Clin Infect Dis. 2005 Nov 15;41 Suppl 7:S504-12. doi: 10.1086/432007.

Abstract

Prominent among the numerous events that contribute to the enhanced susceptibility of elderly patients to infection is the decline of immune function that accompanies aging. Elderly patients experience a marked decline in cell-mediated immune function and reduced humoral immune function. Age-dependent defects in T and B cell function are readily demonstrable in elderly patients, yet the essential elements of innate immunity are remarkably well preserved. The cytokine and chemokine signaling networks are altered in elderly patients and tends to favor a type 2 cytokine response over type 1 cytokine responses. The induction of proinflammatory cytokines after septic stimuli is not adequately controlled by anti-inflammatory mechanisms in elderly persons. This immune dysregulation is accompanied by a more pronounced procoagulant state in older patients. These molecular events function in concert to render elderly patients at excess risk for mortality from severe sepsis and septic shock.

摘要

在导致老年患者易感染的众多因素中,尤为突出的是伴随衰老出现的免疫功能衰退。老年患者的细胞介导免疫功能显著下降,体液免疫功能也降低。在老年患者中,T细胞和B细胞功能随年龄增长出现的缺陷很容易得到证实,然而固有免疫的基本要素却保存得相当完好。老年患者体内的细胞因子和趋化因子信号网络发生了改变,倾向于产生2型细胞因子反应而非1型细胞因子反应。在老年人中,脓毒症刺激后促炎细胞因子的诱导不能通过抗炎机制得到充分控制。这种免疫失调伴随着老年患者更明显的促凝状态。这些分子事件共同作用,使老年患者因严重脓毒症和脓毒性休克而死亡的风险增加。

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