Mediators of Inflammation

Mediators of Inflammation / 2006 / Article

Short Communication | Open Access

Volume 2006 |Article ID 016492 |

Y. Kenan Coban, Murat Aral, "Serum IL-18 Is Increased at Early Postburn Period in Moderately Burned Patients", Mediators of Inflammation, vol. 2006, Article ID 016492, 4 pages, 2006.

Serum IL-18 Is Increased at Early Postburn Period in Moderately Burned Patients

Received24 Jun 2005
Accepted15 Nov 2005
Published12 Mar 2006


A severe systemic inflammatory response is usually seen after burn injury. IL-18 enhances the Th1 immune responses in bacterial andviral infections. In order to evaluate the IL-18 serum levels as well as IL-6 and TNF-α at the 48th hour postburn, serial serum samples of 8 burned patients were analyzed. 8 moderately burned patients were included into the study. Serum samples were taken at admission at the 48th hour of postburn. IL-6, IL-18, and TNF-α serum levels were analyzed. Total mean burned surface area (TBSA) was 24.6±5.7% and mean BMI (body mass index) was 24.5±3.4. The patients' age ranged from 17 to 38 (mean 26.3±7.4) years. An increase in sera IL-6, IL-18, and TNF-α was detected at the 48th hour postburn (P<.0001). All patients survived. A marked increase in serum levels of IL-18 as well as the other cytokines evaluated was observed in the moderately burned patients. These three parameters were highly correlated with each other (r>0.9 and P<.001). This is the first study that shows an increase in serum IL-18 levels at the early postburn period.


  1. M Ueyama, I Maruyama, M Osame, and Y Sawada, “Marked increase in plasma interleukin-6 in burn patients,” The Journal of Laboratory and Clinical Medicine, vol. 120, no. 5, pp. 693–698, 1992. View at: Google Scholar
  2. S Endo, K Inada, Y Yamada et al., “Plasma tumour necrosis factor-α (TNF-α) levels in patients with burns,” Burns, vol. 19, no. 2, pp. 124–127, 1993. View at: Google Scholar
  3. A L Dugan, W B Malarkey, S Schwemberger, E C Jauch, C K Ogle, and N D Horseman, “Serum levels of prolactin, growth hormone, and cortisol in burn patients: correlations with severity of burn, serum cytokine levels, and fatality,” Journal of Burn Care & Rehabilitation, vol. 25, no. 3, pp. 306–313, 2004. View at: Google Scholar
  4. J P de Bandt, S Chollet-Martin, A Hernvann et al., “Cytokine response to burn injury: relationship with protein metabolism,” The Journal of Trauma, vol. 36, no. 5, pp. 624–628, 1994. View at: Google Scholar
  5. F L Yeh, W L Lin, and H D Shen, “Changes in circulating levels of an anti-inflammatory cytokine interleukin 10 in burned patients,” Burns, vol. 26, no. 5, pp. 454–459, 2000. View at: Google Scholar
  6. F L Yeh, W L Lin, H D Shen, and R H Fang, “Changes in circulating levels of interleukin 6 in burned patients,” Burns, vol. 25, no. 2, pp. 131–136, 1999. View at: Google Scholar
  7. F L Yeh, W L Lin, H D Shen, and R H Fang, “Changes in serum tumour necrosis factor-α in burned patients,” Burns, vol. 23, no. 1, pp. 6–10, 1997. View at: Google Scholar
  8. D Takeuchi, H Yoshidome, A Kato et al., “Interleukin 18 causes hepatic ischemia/reperfusion injury by suppressing anti-inflammatory cytokine expression in mice,” Hepatology, vol. 39, no. 3, pp. 699–710, 2004. View at: Google Scholar
  9. F N Lauw, J Branger, S Florquin et al., “IL-18 improves the early antimicrobial host response to pneumococcal pneumonia,” The Journal of Immunology, vol. 168, no. 1, pp. 372–378, 2002. View at: Google Scholar
  10. “American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis,” Critical Care Medicine, vol. 20, no. 6, pp. 864–874, 1992. View at: Google Scholar
  11. K Nakanishi, T Yoshimoto, H Tsutsui, and H Okamura, “Interleukin-18 regulates both Th1 and Th2 responses,” Annual Review of Immunology, vol. 19, pp. 423–474, 2001. View at: Google Scholar
  12. K Nakanishi, T Yoshimoto, H Tsutsui, and H Okamura, “Interleukin-18 is a unique cytokine that stimulates both Th1 and Th2 responses depending on its cytokine milieu,” Cytokine & Growth Factor Reviews, vol. 12, no. 1, pp. 53–72, 2001. View at: Google Scholar
  13. H Okamura, H Tsutsi, T Komatsu et al., “Cloning of a new cytokine that induces IFN-γ production by T cells,” Nature, vol. 378, no. 6552, pp. 88–91, 1995. View at: Google Scholar
  14. S Ushio, M Namba, T Okura et al., “Cloning of the cDNA for human IFN-gamma-inducing factor, expression in Escherichia coli, and studies on the biologic activities of the protein,” The Journal of Immunology, vol. 156, no. 11, pp. 4274–4279, 1996. View at: Google Scholar
  15. A Billiau, “Interferon-gamma: biology and role in pathogenesis,” Advances in Immunology, vol. 62, pp. 61–130, 1996. View at: Google Scholar
  16. W-D Döcke, F Randow, U Syrbe et al., “Monocyte deactivation in septic patients: restoration by IFN-γ treatment,” Nature Medicine, vol. 3, no. 6, pp. 678–681, 1997. View at: Google Scholar
  17. B Conti, J W Jahng, C Tinti, J H Son, and T H Joh, “Induction of interferon-γ inducing factor in the adrenal cortex,” The Journal of Biological Chemistry, vol. 272, no. 4, pp. 2035–2037, 1997. View at: Google Scholar
  18. T Suda, T Takahashi, P Golstein, and S Nagata, “Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family,” Cell, vol. 75, no. 6, pp. 1169–1178, 1993. View at: Google Scholar
  19. A McKay, M Komai-Koma, K J MacLeod et al., “Interleukin-18 levels in induced sputum are reduced in asthmatic and normal smokers,” Clinical & Experimental Allergy, vol. 34, no. 6, pp. 904–910, 2004. View at: Google Scholar
  20. F Giugliano, K Esposito, C Di Palo et al., “Erectile dysfunction associates with endothelial dysfunction and raised proinflammatory cytokine levels in obese men,” Journal of Endocrinological Investigation, vol. 27, no. 7, pp. 665–669, 2004. View at: Google Scholar
  21. H M Wang, W F Cao, Y Z Peng, G X Xiao, and X Y Yang, “Changes in plasma levels of LPS, TNF-α and IL-6 in burn patients with severe infection treated with Imipenem or Cefoperazone,” Zhonghua Shao Shang Za Zhi, vol. 20, no. 2, pp. 95–97, 2004 (Chinese). View at: Google Scholar
  22. M Kinoshita, S Seki, S Ono, N Shinomiya, and H Hiraide, “Paradoxical effect of IL-18 therapy on the severe and mild Escherichia coli infections in burn-injured mice,” Annals of Surgery, vol. 240, no. 2, pp. 313–320, 2004. View at: Google Scholar
  23. M G Netea, G Fantuzzi, B J Kullberg et al., “Neutralization of IL-18 reduces neutrophil tissue accumulation and protects mice against lethal Escherichia coli and Salmonella typhimurium endotoxemia,” The Journal of Immunology, vol. 164, no. 5, pp. 2644–2649, 2000. View at: Google Scholar
  24. B Liu, I Mori, M J Hossain, L Dong, K Takeda, and Y Kimura, “Interleukin-18 improves the early defence system against influenza virus infection by augmenting natural killer cell-mediated cytotoxicity,” Journal of General Virology, vol. 85, no. pt 2, pp. 423–428, 2004. View at: Google Scholar
  25. K Kohno, J Kataoka, T Ohtsuki et al., “IFN-gamma-inducing factor (IGIF) is a costimulatory factor on the activation of Th1 but not Th2 cells and exerts its effect independently of IL-12,” The Journal of Immunology, vol. 158, no. 4, pp. 1541–1550, 1997. View at: Google Scholar

Copyright © 2006 Y. Kenan Coban and Murat Aral. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

More related articles

 PDF Download Citation Citation
 Order printed copiesOrder

Related articles

We are committed to sharing findings related to COVID-19 as quickly as possible. We will be providing unlimited waivers of publication charges for accepted research articles as well as case reports and case series related to COVID-19. Review articles are excluded from this waiver policy. Sign up here as a reviewer to help fast-track new submissions.