• Jun Hur, Hyeong Tae Yang, Wook Chun, Jong-Hyun Kim, Seon-Hee Shin, Hee Jung Kang, and Hyun Soo Kim.
• Department of Burn Surgery, Hallym University Hangang Sacred Heart Hospital, Hallym University College of Medicine, Seoul, Korea.
• Ann Lab Med. 2015 Jan 1; 35 (1): 105-10.

BackgroundMajor burn injuries induce inflammatory responses and changes in the levels of various cytokines. This study was conducted to assess early changes in the serum levels of inflammatory cytokines after burn injury, identify cytokines associated with mortality, and characterize correlations among cytokines.MethodsBlood samples of 67 burn patients were collected on days 1 and 3 after burn injury, and the concentrations of 27 cytokines were measured using the Bio-Plex Suspension Array System (Bio-Rad Laboratories, USA). Blood samples of 25 healthy subjects were used as controls. We analyzed statistical differences in the concentrations of each cytokine between the control and patient groups, between day 1 and day 3, and between survival and nonsurvival groups. Correlations among 27 cytokines were analyzed.ResultsMedian concentrations of granulocyte colony-stimulating factor (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF), interleukin 1 receptor antagonist (IL-1RA), interleukin 6 (IL-6), interleukin 8 (IL-8), interleukin 10 (IL-10), interleukin 15 (IL-15), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein 1β (MIP-1β), and vascular endothelial growth factor (VEGF) were significantly higher in burn patients than in controls. IL-1RA, IL-6, and MCP-1 levels were significantly higher in the nonsurvival group than in the survival group on day 1 after burn injury. Correlation analysis of 27 cytokines showed different relationships with one another. Stronger correlations among interferon γ (IFN-γ), IL-2, IL-4, IL-7, IL-12p70, and IL-17 were found.ConclusionsIL-1RA, IL-6, and MCP-1 may be used as prognostic indicators of mortality in burn patients and the increase in cytokine concentrations is induced by interactions within a complex network of cytokine-related pathways.

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