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[高迁移率族蛋白B1在严重创伤后免疫功能障碍中的潜在作用及其调控机制]

[The potential role of high mobility group box 1 protein in immune dysfunction and its regulatory mechanism after major trauma].

作者信息

Yao Yong-ming, Lin Hong-yuan

机构信息

Emergency and Critical Care Center, First Hospital Affiliated to The Chinese People's Liberation Army General Hospital, Beijing 100037, China.

出版信息

Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2008 Sep;20(9):513-5.

Abstract

OBJECTIVE

To investigate the potential effect of high mobility group box 1 protein (HMGB1) on host immune response and its molecular regulation mechanism as well as its interventional pathway following major burns/trauma.

METHODS

With both animal experiments and clinical investigation, serial studies were conducted to observe the effects of HMGB1 on changes in immune function of T lymphocytes, dendritic cells, and macrophages both in vivo and in vitro.

RESULTS

It was found that thermal injury or trauma induced a delayed and persistent increase in HMGB1 expression as well as its release in various tissues. HMGB1 formation could markedly influence the cell-mediated immunity, including the changes in T lymphocytes, dendritic cells, and macrophages following major trauma or burns. These effects were closely related with dysfunction of various organs in the course of sepsis.

CONCLUSION

These data proved that HMGB1 not only acts as a novel "late" inflammatory mediator but is also closely associated with immunosuppression after acute insults. HMGB1 might play an important role in inducing systemic inflammatory response together with host immunological dissonance, resulting in the development of septic complications. Intervention of HMGB1 expression and release presumably provides a potentially effective way to regulate both excessive inflammatory and immune response, thereby as a measure to improve the prognosis of severe sepsis secondary to major trauma.

摘要

目的

探讨高迁移率族蛋白B1(HMGB1)对严重烧伤/创伤后宿主免疫反应的潜在影响及其分子调控机制和干预途径。

方法

通过动物实验和临床研究,进行系列研究以观察HMGB1在体内外对T淋巴细胞、树突状细胞和巨噬细胞免疫功能变化的影响。

结果

发现热损伤或创伤可导致HMGB1在各种组织中的表达及其释放出现延迟且持续的增加。HMGB1的形成可显著影响细胞介导的免疫,包括严重创伤或烧伤后T淋巴细胞、树突状细胞和巨噬细胞的变化。这些效应与脓毒症过程中各器官功能障碍密切相关。

结论

这些数据证明,HMGB1不仅作为一种新型的“晚期”炎症介质,而且与急性损伤后的免疫抑制密切相关。HMGB1可能在诱导全身炎症反应以及宿主免疫失调中起重要作用,从而导致脓毒症并发症的发生。干预HMGB1的表达和释放可能为调节过度的炎症和免疫反应提供一种潜在有效的方法,从而作为改善严重创伤后继发严重脓毒症预后的一项措施。

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