Dynamics of hepatic gene expression and serum cytokine profiles in single and double-hit burn and sepsis animal models

Abstract

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]).

Endogenous Uteroglobin as Intrinsic Anti-inflammatory Signal Modulates Monocyte and Macrophage Subsets Distribution Upon Sepsis Induced Lung Injury

“…However, the mechanism is still unknown, and it remains to be elucidated whether either direct local tissue injury and the subsequent pro-inflammatory response, or the second hit with excessive pro-inflammatory response and remote organ damage contribute more to the ALI development (41, 60). However, literature indicates that the combination of both hits contributes to the increased pro-inflammatory response following double-hit trauma (61–64). Thus, the question of whether CC16 neutralization would affect the isolated CLP animals in the same way as in the TxT+CLP group remains unanswered.…”

Protective Effects of Melatonin against Severe Burn-Induced Distant Organ Injury: A Systematic Review and Meta-Analysis of Experimental Studies

“…Nuclear factor κB (NF-κB), a transcriptional factor, is activated immediately after severe burn injury and is thought to regulate the expression of several inflammatory mediators, including TNF-α [80]. It has previously been observed that an increase the expression of TNF-α further stimulates for the production of several secondary cytokines, which is considered a crucial pathophysiological mechanism of liver injury following severe burns [81,82]. Interestingly, the liver is one of the most prone organs to inflammatory damage in thermal injury [83].…”