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双重打击烧伤和脓毒症动物模型中早期炎症反应的动力学。

The dynamics of the early inflammatory response in double-hit burn and sepsis animal models.

机构信息

Department of Chemical and Biochemical Engineering, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.

出版信息

Cytokine. 2011 Nov;56(2):494-502. doi: 10.1016/j.cyto.2011.07.001. Epub 2011 Aug 6.

DOI:10.1016/j.cyto.2011.07.001
PMID:21824784
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3185215/
Abstract

Severe burn trauma is generally associated with bacterial infections, which causes a more persistent inflammatory response with an ongoing hypermetabolic and catabolic state. This complex biological response, mediated by chemokines and cytokines, can be more severe when excessive interactions between the mediators take place. In this study, the early inflammatory response following the cecum ligation and puncture (CLP) or its corresponding control treatment (sham-CLP or SCLP) in burn (B) male rats was analyzed by measuring 23 different cytokines and chemokines. Cytokines and chemokines, including MCP-1, IP-10, leptin, TNF-α, MIP-1α, IL-18, GMCSF, RANTES and GCSF were significantly altered in both B+CLP and B+SCLP groups. IL-10 and IL-6 were significantly up-regulated in the B+CLP group when compared to the B+SCLP group. Down regulation of leptin and IP-10 concentrations were found to be related to surgery and/or infection. IL-18 and MCP-1 were elevated in all groups including previously published single injury models receiving similar treatments. In this study, insult-specific mediators with their characteristic temporal patterns were elucidated in double hit models.

摘要

严重烧伤创伤通常与细菌感染有关,这会导致持续的代谢亢进和分解代谢状态,引起更持久的炎症反应。这种由趋化因子和细胞因子介导的复杂生物学反应,如果介质之间发生过度相互作用,可能会更加严重。在这项研究中,通过测量 23 种不同的细胞因子和趋化因子,分析了烧伤(B)雄性大鼠盲肠结扎和穿刺(CLP)或其相应对照治疗(假 CLP 或 SCLP)后的早期炎症反应。MCP-1、IP-10、瘦素、TNF-α、MIP-1α、IL-18、GMCSF、RANTES 和 GCSF 等细胞因子和趋化因子在 B+CLP 和 B+SCLP 组中均发生明显改变。与 B+SCLP 组相比,B+CLP 组中 IL-10 和 IL-6 明显上调。瘦素和 IP-10 浓度的下调与手术和/或感染有关。IL-18 和 MCP-1 在所有包括之前发表的接受类似治疗的单一损伤模型的组中均升高。在这项研究中,在双重打击模型中阐明了具有特征性时间模式的损伤特异性介质。

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