Rao Rohit, Orman Mehmet A, Berthiaume Francois, Androulakis Ioannis P
Department of Chemical and Biochemical Engineering, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.
Chemical and Biological Engineering Department, Princeton University, Princeton, NJ 08544, USA.
Data Brief. 2015 Mar 11;3:229-33. doi: 10.1016/j.dib.2015.02.018. eCollection 2015 Jun.
We simulate the pathophysiology of severe burn trauma and burn-induced sepsis, using rat models of experimental burn injury and cecal ligation and puncture (CLP) either individually (singe-hit model) or in combination (double-hit model). The experimental burn injury simulates a systemic but sterile pro-inflammatory response, while the CLP simulates the effect of polymicrobial sepsis. Given the liver׳s central role in mediating the host immune response and onset of hypermetabolism after burn injury, elucidating the alterations in hepatic gene expression in response to injury can lead to a better understanding of the regulation of the inflammatory response, whereas circulating cytokine protein expression, reflects key systemic inflammatory mediators. In this article, we present both the hepatic gene expression and circulating cytokine/chemokine protein expression data for the above-mentioned experimental model to gain insights into the temporal dynamics of the inflammatory and hypermetabolic response following burn and septic injury. This data article supports results discussed in research articles (Yang et al., 2012 [1,4]; Mattick et al. 2012, 2013 [2,3]; Nguyen et al., 2014 [5]; Orman et al., 2011, 2012 [6-8]).
我们利用实验性烧伤损伤大鼠模型和盲肠结扎穿孔（CLP）模型，单独（单次打击模型）或联合（双次打击模型）模拟严重烧伤创伤和烧伤诱导的脓毒症的病理生理学。实验性烧伤损伤模拟全身性但无菌的促炎反应，而CLP模拟多微生物脓毒症的影响。鉴于肝脏在介导烧伤后宿主免疫反应和高代谢发作中的核心作用，阐明肝脏基因表达对损伤的反应变化可以更好地理解炎症反应的调节，而循环细胞因子蛋白表达反映了关键的全身炎症介质。在本文中，我们展示了上述实验模型的肝脏基因表达和循环细胞因子/趋化因子蛋白表达数据，以深入了解烧伤和脓毒症损伤后炎症和高代谢反应的时间动态。本数据文章支持研究文章（Yang等人，2012 [1,4]；Mattick等人，2012年，2013年 [2,3]；Nguyen等人，2014年 [5]；Orman等人，2011年，2012年 [6-8]）中讨论的结果。
