Burns and trauma lead to a hypermetabolic state characterized by an accelerated breakdown of skeletal muscle protein in the patient which leads to muscle wasting and reduction of lean body Since burn patients in general experience a breakdown in gut barrier function that causes bacterial translocation into the body, patients that develop septic complications exhibit a prolonged hypermetabolic state which is triggered by a systematic inflammatory response. This inflammatory response is mediated by circulatory cytokines or proteins, which in turn might affect the signal transduction in liver resulting in changes in gene expression profiles, which plays an important role in hypermetabolic state. Although some inflammatory cytokines expressed in liver or circulated in the blood, such as IL1-â, IL-2, IL-6, IL-10 and TNF-á, have been extensively studied following thermal injuries (Gauglitz et al. 2008; Klein et al. 2003; Summer et al. 2008), more comprehensive analysis given the dynamic behaviors of all possible inflammatory proteins after burn injury or sepsis is required. The purpose of this study is to characterize concentration changes in circulatory proteins or cytokines (Eotaxin, G-CSF, GM-CSF, GRO/KC, IFN-ã, IL-10, IL-12 (p70), IL-13, IL-17, IL-18, IL-1á, IL-1â, IL-2, IL-4, IL-5, IL-6, IP-10, Leptin, MCP-1, MIP-1á, RANTES, TNF-á, VEGF) at different time points after burn injury and/or superimposed infection to identify initial (0.5 h, 1h, 1.5h, 2), short term (2 h, 4 h, 8 h, 16h, 24h) and long term inflammatory response (1 day, 2 day, 3 day, 4 day, 7 day, 10 day). This study is conducted using rat models of burn injury and infection. A systemic hypermetabolic response was induced in rats by applying a 20 % total body surface area burn followed by (2 days later) cecal ligation and puncture (CLP) to produce sepsis. Control groups are treated identically except that they are given a sham-burn using 37 C water or sham-CLP, the survival surgical procedure without any puncture in cecum. An extensive description of circulating protein or cytokine profiles will give the key aspects of inflammation such as pro-inflammation, anti-inflammation, and post-inflammation. This also provides an in-slico model of acute inflammation in the liver that combines the extracellular signals, i.e. circulatory proteins and cytokines, with essential transcriptional responses obtained from microarray analysis. References Gauglitz GG, Song J, Herndon DN, Finnerty CC, Boehning D, Barral JM, Jeschke MG. 2008. Characterization of the Inflammatory Response During Acute and Post-Acute Phases after Severe Burn. Shock 30(5):503-507. Klein D, Einspanier R, Bolder U, Jeschke MG. 2003. Differences in the hepatic signal transcription pathway and cytokine expression between thermal injury and sepsis. Shock 20(6):536-543. Summer GJ, Romero-Sandoval EA, Bogen O, Dina OA, Khasar SG, Levine JD. 2008. Proinflammatory cytokines mediating burn-injury pain. Pain 135(1-2):98-107.
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