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创伤/出血和创伤性脑损伤中的急性炎症反应:现状与新展望。

The acute inflammatory response in trauma / hemorrhage and traumatic brain injury: current state and emerging prospects.

机构信息

Department of Surgery.

出版信息

Libyan J Med. 2009 Sep 1;4(3):97-103. doi: 10.4176/090325.

Abstract

Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.

摘要

创伤性损伤/失血性休克(T/HS)会引发急性炎症反应,可能导致死亡。炎症描述了一系列协调的分子、细胞、组织、器官和全身反应,导致包括 T/HS 和创伤性脑损伤(TBI)在内的各种疾病的病理变化。炎症是一个精细调节、动态、高度调节的过程,它本身并不是有害的,而是免疫监视、最佳损伤后组织修复和再生所必需的。炎症反应由细胞因子和趋化因子驱动,部分由受损组织衍生产物(损伤相关分子模式;DAMP's)传播。DAMPs 通过释放促炎细胞因子来持续引发炎症,但也可能抑制抗炎细胞因子。已经在小鼠、大鼠、猪、狗和非人类灵长类动物中使用了各种 T/HS 的动物模型,试图从实验室走向临床。包括系统生物学领域在内的新方法可能在不久的将来为 T/HS 和 TBI 带来治疗突破。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc64/3066737/ad77404b36d1/LJM-4-097-g001.jpg

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