NOVEL HMGB1-INHIBITING THERAPEUTIC AGENTS FOR EXPERIMENTAL SEPSIS

被引：124

作者：

Wang, Haichao ^{[1
,2
]}

Ward, Mary F. ^{[2
]}

Sama, Andrew E. ^{[2
]}

机构：

[1] N Shore LIJ Hlth Syst, Feinstein Inst Med Res, Manhasset, NY 11030 USA

[2] NYU, Sch Med, N Shore Univ Hosp, Dept Emergency Med, Manhasset, NY USA

来源：

SHOCK | 2009年 / 32卷 / 04期

基金：

美国国家卫生研究院;

关键词：

Innate immune cells; phagocytes; inflammation; cytokines; sepsis; antibodies; HMGB1; tanshinones; MOBILITY GROUP BOX-1; NECROSIS-FACTOR-ALPHA; GRAM-NEGATIVE BACTEREMIA; CHROMATIN PROTEIN HMGB1; GLYCATION END-PRODUCTS; ACUTE LUNG INJURY; HIGH-MOBILITY-GROUP-BOX-1; PROTEIN; LETHAL SEPSIS; SEPTIC SHOCK; MONOCLONAL-ANTIBODY;

D O I：

10.1097/SHK.0b013e3181a551bd

中图分类号：

R4 [临床医学];

学科分类号：

1002 ; 100602 ;

摘要：

Sepsis refers to a systemic inflammatory response syndrome resulting from a microbial infection. The inflammatory response is partly mediated by innate immune cells (such as macrophages, monocytes, and neutrophils), which not only ingest and eliminate invading pathogens but also initiate an inflammatory response by producing early (e.g., TNF and IFN-gamma and late (e.g., high-mobility group box [HMGB1]) proinflammatory cytokines. Here, we briefly review emerging evidence that support extracellular HMGB1 as a late mediator of experimental sepsis and discuss therapeutic potential of several HMGB1-inhibiting agents (including neutralizing antibodies and steroid-like tanshinones) in experimental sepsis.

引用

页码：348 / 357

页数：10

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