Finnerty CC, Herndon DN, Przkora R et al.Cytokine expression profile over time in severely burned pediatric patients. Shock 26:13-19

Texas A&M University - Galveston, Galveston, Texas, United States
Shock (Impact Factor: 3.05). 07/2006; 26(1):13-9. DOI: 10.1097/01.shk.0000223120.26394.7d
Source: PubMed


A severe burn leads to hypermetabolism and catabolism resulting in compromised function and structure of essential organs. The massive release of cytokines is implicated in this hypermetabolic response. The aim of the present study was to compare cytokine expression profiles from severely burned children without signs of infections or inhalation injury (n = 19) to the cytokine profiles from normal, noninfected, nonburned children (n = 14). The Bio-Plex suspension array system was used to measure the concentration of 17 cytokines. The expression of proinflammatory and anti-inflammatory cytokines was maximal during the first week after thermal injury. Significant increases were measured for 15 mediators during the first week after thermal injury: interleukin (IL) 1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12 p70, IL-13, IL-17, interferon gamma, monocyte chemoattractant protein 1, macrophage inflammatory protein 1beta, and granulocyte colony-stimulating factor (P < 0.05). Granulocyte-macrophage colony-stimulating factor was significantly increased during the second week after burn (P < 0.05). Within 5 weeks, the serum concentrations of most cytokines decreased, approaching normal levels. When compared with the cytokine levels measured in normal children, a total of 16 cytokines were significantly altered (P < 0.05). After severe burn, a specific cytokine expression profile is observed in patients without complications such as inhalation injury or sepsis. The cytokine concentrations decrease during 5 weeks after burn but remain elevated over nonburned values. Furthermore, the elevation in most serum cytokine levels during the first week after burn may indicate a potential window of opportunity for therapeutic intervention.

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    • "Severe burns generally associated with systemic inflammatory response syndrome (SIRS) with attributed alteration of proinflammatory and anti-inflammatory cytokines in the early postinsult period [8] [9]. Cytokines and growth factors can influence the expression of MMPs and TIMPs significantly [10], and therefore, the balance of MMP-TIMP system could be altered during the early postinjury period. "
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    ABSTRACT: Purpose: Severe burn is a life-threatening condition. Many trials discuss the role of matrix metalloproteinases and tissue inhibitor of metalloproteinases in diseases generating systemic inflammatory response syndrome, and in some, their prognostic importance has been established. We aimed to describe the time courses of the aforementioned system and to evaluate the difference between survivors and nonsurvivors in burns. Materials: Thirty-one patients were enrolled. Blood samples were collected on admission and on the 5 consecutive days. Circulating matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) have been measured. Healthy individuals were invited as controls. Results: Tissue inhibitor of metalloproteinase 1 increased in the burn group (P < .001) by day 2 and remained elevated thereafter. Plasma MMP-9 and MMP-9/TIMP-1 were already elevated on admission (P < .001) and decreased in tendency thereafter. In burned patients, significantly lower MMP-9 were noted on days 4 to 6 as MMP-9/TIMP-1 were also lower on days 3 to 6 (P < .01) compared with controls. We experienced difference regarding survival on days 5 and 6 by TIMP-1 (P < .05). Conclusions: Our research is the first follow-up study elucidating the dynamic changes of MMP-9-TIMP-1 system in severe burns. Alteration of MMP-9-TIMP-1 balance might influence systemic inflammatory response and related mortality. Matrix metalloproteinase 9 might be a good injury marker in burns after an extensive trial.
    Full-text · Article · Jul 2014 · Journal of Critical Care
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    • "The pathophysiological response to thermal trauma is multifactorial with resulting perturbations in metabolism affecting nearly every physiological system [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16]. Like most forms of critical illness, severe burns result in an inflammatory and hypermetabolic stress response, but the extent and duration of these responses and their debilitating nature appear unique to burn trauma [1,6,7,17–20]. "
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    ABSTRACT: Severe burns induce a pathophysiological response that affects almost every physiological system within the body. Inflammation, hypermetabolism, muscle wasting, and insulin resistance are all hallmarks of the pathophysiological response to severe burns, with perturbations in metabolism known to persist for several years post injury. Skeletal muscle is the principal depot of lean tissue within the body and as the primary site of peripheral glucose disposal, plays an important role in metabolic regulation. Following a large burn, skeletal muscle functions as and endogenous amino acid store, providing substrates for more pressing functions, such as the synthesis of acute phase proteins and the deposition of new skin. Subsequently, burn patients become cachectic, which is associated with poor outcomes in terms of metabolic health and functional capacity. While a loss of skeletal muscle contractile proteins per se will no doubt negatively impact functional capacity, detriments in skeletal muscle quality, i.e. a loss in mitochondrial number and/or function may be quantitatively just as important. The goal of this review article is to summarise the current understanding of the impact of thermal trauma on skeletal muscle mitochondrial content and function, to offer direction for future research concerning skeletal muscle mitochondrial function in patients with severe burns, and to renew interest in the role of these organelles in metabolic dysfunction following severe burns.
    Full-text · Article · May 2013 · Burns: journal of the International Society for Burn Injuries
    • "Also, the expression of IL-1β was decreased compared to control group. These results suggest that acupuncture stimulation may have protective effects in wound model through the suppression of pro-inflammatory cytokines, which are secreted by macrophages [19, 20]. "
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    ABSTRACT: Acupuncture regulates inflammation process and growth factors by increasing blood circulation in affected areas. In this study, we examined whether acupuncture has an effect on wound healing in injured rat. Rats were assigned randomly into two groups: control group and acupuncture group. Acupuncture treatment was carried out at 8 sites around the wounded area. We analyzed the wound area, inflammatory cytokines, proliferation of resident cells, and angiogenesis and induction of extracelluar matrix remodeling. At 7 days after-wounding the wound size in acupuncture-treat group was decreased more significantly compared to control group. In addition, the protein levels of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were significantly decreased compared to the control at 2 and 7 days post-wounding. Also, we analyzed newly generated cells by performing immunostaining for PCNA and using several phenotype markers such as CD-31, α-SMA, and collagen type I. In acupuncture-treated group, PCNA-positive cell was increased and PCNA labeled CD-31-positive vessels, α-SMA- and collagen type I-positive fibroblastic cells, were increased compared to the control group at 7 days post-wounding. These results suggest that acupuncture may improve wound healing through decreasing pro-inflammatory response, increasing cell proliferation and angiogenesis, and inducing extracellular matrix remodeling.
    No preview · Article · Dec 2012 · Evidence-based Complementary and Alternative Medicine
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