Investigation of the course of proinflammatory and anti-inflammatory cytokines after burn sepsis

Abstract

Cytokines have been considered as important participants in the post-burn pathophysiological process. The aim of this study was to investigate the course of a proinflammatory cytokine interleukin-8 (IL-8) and an anti-inflammatory cytokine IL-10 in burned patients and whether there was a correlation between mortality and serum levels of these cytokines. Thirty-six acutely burned patients, admitted to Ankara Numune hospital burn unit, entered into the study. A series of serum samples were collected, and serum levels of IL-8 and IL-10 were determined using enzyme-linked immunosorbent assay kit. According to definition utilised, 21 patients developed septic shock and nine of them died. There was no mortality among the 17 non-septic patients. In all 36 patients, there was an increase in serum IL-8 levels, and a peak level was detected shortly after burn injury. The peak IL-8 value of the non-survivors was greater when compared with that of the others. On admission, a significant difference in serum IL-8 values was found between survivors and those who died. In all patients, a peak level of IL-10 was detected between 5 and 9 days of injury. In non-septic survivors, this peak level was less when compared with that of the others. After this peak level, in all patients, serum IL-10 levels showed a decrease, but in non-survivors, a second peak level was detected. A greater understanding of the pathology of the burn sepsis allows rationale use and assessment of current therapies. The results obtained in this study provide useful information on the formulation approaches to this task. Also, IL-8 and IL-10 are prognostic factors in burn sepsis.

Clinical Evaluation of Proinflammatory Cytokine Inhibitors (sTNFR I, sTNFR II, IL‐1 ra), Anti‐inflammatory Cytokines (IL‐10, IL‐13) and Activation of Neutrophils after Burn‐induced Inflammation

“…soluble TNF-a receptors and IL-1 ra) [4,29,30]. Additionally, IL-10 may stimulate the synthesis of IL-1ra enhancing the host anti-inflammatory response in SIRS development, which may be confirmed by the positive significant correlation between the levels of IL-1 ra and IL-10 observed in our patients within the first 6-24 h after burn.…”

“…There are intensive studies assessing neutrophil priming, cytokine levels and their inhibitors in the blood of patients fulfilling SIRS criteria in the course of various clinical entities [4,5,10,15,20,21]. Priming occurs in vivo during SIRS and it enhances the capacity of neutrophils to kill micro-organisms as well as damage normal tissue.…”

“…Several studies have shown disturbances in innate and adaptive immune response as a consequence of burns, accident trauma and surgical operation -major surgery often leads to severe immunosuppression that is characterized by impaired cell-mediated immune response. In the complex pathogenesis of burns, interest has been evinced on the proinflammatory cytokines, released by activated macrophages and reactive oxygen species (ROS), which are produced in the course of the 'so-called' respiratory burst of neutrophils [4,5,[7][8][9][10][14][15][16]. Due to difficulties in reproducing the presence and results of ROS activity in vivo (as they have a very short half-life), the role of ROS in the pathomechanism of SIRS in patients after thermal injury is still not well documented.…”

“…Systemic disorders result in the development of the systemic inflammatory response syndrome (SIRS) that is the clinical expression of the action of complex intrinsic mediators of the acute phase reaction. Proinflammatory cytokines are considered endogenic mediators demonstrating immunomodulating activity, which occur in the course of SIRS and are involved in the systemic response to infection or a noninfectious factor [1][2][3][4][5]. This process leads to tissue and organ impairment in the course of the so-called oxidative stress that can be observed in SIRS cases with concomitant equilibrium disturbances between oxygen free radical generation and the process of their inactivation [6][7][8][9].…”

“…IL-4, IL-13, IL-10 that inhibit proinflammatory cytokine production) and in release of circulating soluble receptors or receptor antagonists. Numerous studies have reported the presence of cytokine inhibitors for tumour necrosis factor-a (TNF-a), interleukin (IL)-1, IL-6 as well as anti-inflammatory cytokines in patients with a systemic inflammatory process or severe injury [2,4,[10][11][12][13].…”