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Chinese Burn Surgery pp 89–106Cite as

Bacterial Endotoxin and Exotoxin in Severe Burns

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Abstract

The pathological mechanisms underlying the development of multiple organ dysfunction syndrome (MODS) in critically ill patients remain poorly understood. Nevertheless, the most widely held view is that uncontrolled systemic activation of the inflammatory response somehow leads to cellular dysfunction and/or destruction at locations distant from the initiating site(s) of injury or infection. Complications that occur during sepsis and MODS are ultimately the consequence of an overreaction of host defense mechanisms to bacterial infection. The reaction is the so-called generalized inflammatory response, which is an essential reaction of the host to both burns/trauma and septic episode [1]. When overactivated, the systemic inflammatory response can be against the host in a self-destructive manner. While the initial inflammatory response can be initiated both by extensive burns and sepsis, the perpetuation of the response is usually associated with bacterial component. One of the central principles by which bacteria induce the inflammatory response and subsequent organ dysfunction is via bacterial toxins, of which endotoxin or lipopolysaccharide (LPS) from gram-negative bacteria is the most prominent. Endotoxin, a cell wall component of gram-negative bacteria, is known to activate the cytokine pathways that lead to the release of proinflammatory mediators, which results in a wide range of pathophysiological effects. Recent advances in molecular biology and mostly immunology have greatly contributed to our understanding of the pathophysiology of sepsis not only by endotoxin but also by other microbial products, including exotoxin mainly from gram-positive bacteria [2]. Infections begin when bacteria penetrate host barriers such as the skin and mucosa, sometimes overwhelming host defenses and releasing toxic bacterial products that activate plasma factors (complement and clotting molecules) as well as cells of the immune system. The result is that the host’s inflammatory response contributes substantially to the development of sepsis and MODS secondary to severe burns/trauma.

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References

  1. Yao YM, Redl H, Bahrami S, et al. The inflammatory basis of trauma/shock associated multiple organ failure. Inflamm Res. 1998;47:201–10.

    Article  CAS  PubMed  Google Scholar 

  2. Shiranee S, Cohen J. Gram-positive sepsis: mechanisms and differences from gram-negative sepsis. Infect Dis Clin N Am. 1999;13:397–412.

    Article  Google Scholar 

  3. Swank GM, Deitch EA. Role of the gut in multiple organ failure: bacterial translocation and permeability changes. World J Surg. 1996;20:411–7.

    Article  CAS  PubMed  Google Scholar 

  4. Xiao GX. Pay more attention on endogenous infection. Chin Plast Burns Surg. 1996;12:81–2.

    CAS  Google Scholar 

  5. Yao YM, Bahrami S, Leichtfried G, et al. Pathogenesis of hemorrhage-induced bacteria/endotoxin translocation in rats: effects of recombinant bactericidal/permeability-increasing protein. Ann Surg. 1995;221:398–405.

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  6. Fang WH, Yao YM, Shi ZG, et al. Effect of recombinant bactericidal/permeability-increasing protein on endotoxin translocation and lipopolysaccharide-binding protein/CD14 expression in rats following thermal injury. Crit Care Med. 2001;29:1452–9.

    Article  CAS  PubMed  Google Scholar 

  7. Deitch EA. Multiple organ failure: pathophysiology and potential future therapy. Ann Surg. 1992;216:117–34.

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  8. Rush BFJ, Sori AJ, Murphy TF, et al. Endotoxemia and bacteremia during hemorrhagic shock: the link between trauma and sepsis? Ann Surg. 1988;207:549–54.

    Article  PubMed Central  PubMed  Google Scholar 

  9. Yao YM, Wang YP, Tian HM, et al. Reduction of circulating prostaglandin E2 level by antiserum against core lipopolysaccharide in a rabbit model of multiple organ failure. J Trauma. 1996;40:270–7.

    Article  CAS  PubMed  Google Scholar 

  10. Yao YM, Yu Y, Sheng ZY, et al. Role of gut-derived endotoxemia and bacterial translocation in rats after thermal injury: effects of selective decontamination of the digestive tract. Burns. 1995;21:580–5.

    Article  CAS  PubMed  Google Scholar 

  11. Fang WH, Yao YM, Shi ZG, et al. The time course and tissue distribution of endotoxin translocation in rats after thermal injury. Chin Plast Burns Surg. 1999;15:298–300.

    CAS  Google Scholar 

  12. Sheng ZY, Yao YM, Yu Y. The relationship between gut-derived endotoxemia and tumor necrosis factor, neopterin: experimental and clinical studies. Chin Med J. 1997;110:30–5.

    CAS  PubMed  Google Scholar 

  13. Yao YM, Sheng ZY, Tian HM, et al. The association of circulating endotoxemia with the development of multiple organ failure in burned patients. Burns. 1995;21:255–8.

    Article  CAS  PubMed  Google Scholar 

  14. Yao YM, Bahrami S, Redl H, et al. Monoclonal antibody to tumor necrosis factor-α attenuates hemodynamic dysfunction secondary to intestinal ischemia/reperfusion in rats. Crit Care Med. 1996;24:1547–53.

    Article  CAS  PubMed  Google Scholar 

  15. Yao YM, Sheng ZY, Yu Y, et al. The potential etiologic role of tumor necrosis factor in mediating multiple organ dysfunctions in rats following intestinal ischemia-reperfusion injury. Resuscitation. 1995;29:157–68.

    Article  CAS  PubMed  Google Scholar 

  16. Yao YM, Tian HM, Sheng ZY, et al. Inhibitory effects of low-dose polymyxin B on hemorrhage-induced endotoxin/bacterial translocation and cytokine formation. J Trauma. 1995;38:924–30.

    Article  CAS  PubMed  Google Scholar 

  17. Chen G, Ward MF, Sama AE, et al. Extracellular HMGB1 as a proinflammatory cytokine. J Interferon Cytokine Res. 2004;24:329–33.

    Article  PubMed  Google Scholar 

  18. Yao YM, Sheng ZY, Huang LF. The effect of a novel cytokine, high mobility group box 1 protein, on the development of traumatic sepsis. Chin J Integr Med. 2009;15:13–5.

    Article  PubMed  Google Scholar 

  19. Zhang LT, Yao YM, Lu JQ, et al. Sodium butyrate prevents lethality of severe sepsis in rats. Shock. 2007;27:672–7.

    Article  CAS  PubMed  Google Scholar 

  20. Liu H, Yao YM, Yu Y, et al. Role of Janus kinase/signal transducer and activator of transcription pathway in regulation of expression and inflammation-promoting activity of high mobility group box protein 1 in rat peritoneal macrophages. Shock. 2007;27:55–60.

    Article  PubMed  Google Scholar 

  21. Fang WH, Yao YM, Shi ZG, et al. The significance of changes in high mobility group-1 protein mRNA expression in rats after thermal injury. Shock. 2002;17:329–33.

    Article  PubMed  Google Scholar 

  22. Dong N, Yao YM, Yu Y, et al. Changes in plasma high mobility group box-1 protein levels in severely burned patients. Acta Acad Med Sinicae. 2007;29:466–70.

    CAS  Google Scholar 

  23. Bahrami S, Yao YM, Leichtfried G, et al. Monoclonal antibody to endotoxin attenuates hemorrhage-induced lung injury and mortality in rats. Crit Care Med. 1997;25:1030–6.

    Article  CAS  PubMed  Google Scholar 

  24. Boermeester MA, Houdijk AP, Meyer S, et al. Liver failure induces a systemic inflammatory response: prevention by recombinant N-terminal bactericidal/permeability-increasing protein. Am J Pathol. 1995;147:1428–40.

    CAS  PubMed Central  PubMed  Google Scholar 

  25. Yao YM, Yu Y, Wu Y, et al. Role of the gut as a cytokine-generating organ in remote organ dysfunction after intestinal ischemia and reperfusion. Chin Med J. 1998;111:514–8.

    CAS  PubMed  Google Scholar 

  26. Rhee P, Waxman K, Clark L, et al. Tumor necrosis factor and monocytes are released during hemorrhagic shock. Resuscitation. 1993;25:249–55.

    Article  CAS  PubMed  Google Scholar 

  27. Yao YM, Yu Y, Sheng ZY, et al. The effect of intestinal ischemia/reperfusion on increased sensitivity to endotoxin and its potential mechanism. Chin Plast Burns Surg. 1999;15:301–4.

    CAS  Google Scholar 

  28. Williams JG, Bankey P, Minei JP, et al. Burn injury enhances alveolar macrophage endotoxin sensitivity. J Burn Care Rehabil. 1994;15:493–8.

    Article  CAS  PubMed  Google Scholar 

  29. Kitchens RL, Tex D. Role of CD14 in cellular recognition of bacterial lipopolysaccharide. Chem Immunol. 2000;74:61–82.

    Article  CAS  PubMed  Google Scholar 

  30. Perera PY, Mayadas TN, Takeuchi O, et al. CD11b/CD18 acts in concert with CD14 and Toll-like receptor (TLR) 4 to elicit full lipopolysaccharide and taxol-inducible gene expression. J Immunol. 2001;166:574–81.

    Article  CAS  PubMed  Google Scholar 

  31. Yao YM, Yu Y, Lu LR, et al. Increased soluble CD14 levels correlate with endotoxemia in critical patients with multiple organ failure. In: Faist E, editor. The immune consequences of trauma, shock and sepsis: mechanisms and therapeutic approaches. Bologna: Moduzzi Editore; 1997. p. 149–54.

    Google Scholar 

  32. Fang WH, Yao YM, Shi ZG, et al. Lipopolysaccharide-binding protein and lipopolysaccharide receptor CD14 gene expression after thermal injury and its potential mechanism(s). J Trauma. 2002;53:957–67.

    Article  CAS  PubMed  Google Scholar 

  33. Ishii Y, Shuyi W, Kitamura S. Soluble CD14 in serum mediates LPS-induced increase in permeability of bovine pulmonary arterial endothelial cell monolayer in vitro. Life Sci. 1995;56:2263–72.

    Article  CAS  PubMed  Google Scholar 

  34. Yao YM, Zhang LT, Lu JQ, et al. The changes in tissue lipopolysaccharide-binding protein/CD14 mRNA expression and their relation to high mobility group-1 induction in septic rats. Chin J Traum. 2002;18:540–3.

    CAS  Google Scholar 

  35. Yao YM, Lu LR, Yu Y, et al. The influence of selective decontamination of the digestive tract on cell-mediated immune function and bacteria/endotoxin translocation in thermally injured rats. J Trauma. 1997;42:1073–9.

    Article  CAS  PubMed  Google Scholar 

  36. Munster MA, Winchurch RA, Thupari JN, et al. Reversal of postburn immunosuppression with low-dose polymyxin B. J Trauma. 1986;26:995–1001.

    Article  CAS  PubMed  Google Scholar 

  37. Hotchkiss RS, Karl JE. The pathophysiology and treatment of sepsis. N Engl J Med. 2003;348:138–50.

    Article  CAS  PubMed  Google Scholar 

  38. Li HY, Yao YM, Shi ZG, et al. Significance of biopterin induction in rats with postburn Staphylococcus aureus sepsis. Shock. 2003;20:159–65.

    Article  CAS  PubMed  Google Scholar 

  39. Yao YM, Yu Y, Wang YP, et al. Elevated serum neopterin level: its relation to endotoxemia and sepsis in patients with major burns. Eur J Clin Invest. 1996;26:224–30.

    Article  CAS  PubMed  Google Scholar 

  40. Cohen J. The detection and interpretation of endotoxemia. Intensive Care Med. 2000;26:S51–6.

    Article  PubMed  Google Scholar 

  41. Yao YM, Tian HM, Wang YP, et al. Protective effect of Re-LPS antiserum on experimental multiple system organ failure. Chin Med J. 1992;105:833–8.

    CAS  PubMed  Google Scholar 

  42. Yao YM, Tian HM, Sheng ZY, et al. The role of endotoxin in the pathogenesis of experimental multiple system organ failure: a preliminary report. Chin Med Sci J. 1992;7:161–5.

    CAS  PubMed  Google Scholar 

  43. Endo S, Inada K, Kikuchi M, et al. Are plasma endotoxin levels related to burn size and prognosis? Burns. 1992;18:486–90.

    Article  CAS  PubMed  Google Scholar 

  44. Levy O. Therapeutic potential of the bactericidal/permeability-increasing protein. Expert Opin Investig Drugs. 2002;11:159–67.

    Article  CAS  PubMed  Google Scholar 

  45. Zhang LT, Yao YM, Lu JQ, et al. Recombinant bactericidal/permeability-increasing protein inhibits endotoxin-induced high mobility group box 1 protein gene expression in sepsis. Shock. 2008;29:278–84.

    Article  PubMed  Google Scholar 

  46. Dellinger PR, Levy MM, Carlet JM, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock 2008. Crit Care Med. 2008;36:296–327.

    Article  PubMed  Google Scholar 

  47. de Jonge E, Schultz M, Spanjarrd L, et al. Selective decontamination of the digestive tract in intensive care. Lancet. 2003;362:2119–20.

    Article  Google Scholar 

  48. Russell JA. Management of sepsis. N Engl J Med. 2006;355:1699–713.

    Article  CAS  PubMed  Google Scholar 

  49. Yao YM, Sheng ZY. Modern opinions on signal transduction in sepsis. Chin Crit Care Med. 2003;15:3–6.

    Google Scholar 

  50. Sheagren JN. Staphylococcus aureus infections in trauma patients. Crit Care Med. 1999;27:692–3.

    Article  CAS  PubMed  Google Scholar 

  51. Balaban N, Rasooly A. Staphylococcal enterotoxins. Int J Food Microbiol. 2000;61:1–10.

    Article  CAS  PubMed  Google Scholar 

  52. Cameron SB, Nawijn MC, Kum WW, et al. Regulation of helper T cell responses to staphylococcal super-antigen. Eur Cytokine Netw. 2001;12:210–22.

    CAS  PubMed  Google Scholar 

  53. Wray GM, Foster SJ, Hinds CJ, et al. A cell wall component from pathogenic and non-pathogenic gram-positive bacteria (peptidoglycan) synergises with endotoxin to cause the release of tumor necrosis factor-alpha, nitric oxide production, shock, and multiple organ injury/dysfunction in rat. Shock. 2001;15:135–42.

    Article  CAS  PubMed  Google Scholar 

  54. Shi ZG, Yu Y, Yao YM, et al. The potential role of staphylococcal enterotoxin B in the development of multiple organ injury in rabbits. J Hyg Res. 1998;27:187–8.

    Google Scholar 

  55. Li HY, Yao YM, Shi ZG, et al. The potential role of Staphylococcal enterotoxin B in rats with postburn Staphylococcus aureus sepsis. Shock. 2003;20:257–63.

    Article  CAS  PubMed  Google Scholar 

  56. Stiles BG, Garza AR, Ulrich RG, et al. Mucosal vaccination with recombinantly attenuated staphylococcal enterotoxin B and protection in a murine model. Infect Immun. 2001;69:2031–6.

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  57. Yao YM, Sheng ZY. Staphylococcal enterotoxin B and multiple organ dysfunction syndrome. Chin Crit Care Med. 2001;13:517–9.

    Google Scholar 

  58. Yao YM, Xu S, Sheng ZY. Advances in high mobility group box-1 protein mediated multiple organ dysfunction and its potential interventional strategies. Acta Acad Med Sinicae. 2007;29:459–65.

    CAS  Google Scholar 

  59. Li HY, Yao YM, Shi ZG, et al. Significance of changes in high mobility group-1 protein in rats with postburn Staphylococcus aureus sepsis. Chin J Exp Surg. 2001;18:336–7.

    Google Scholar 

  60. Liu H, Yao YM, Wang SB, et al. Inhibition of Janus kinase 2 and signal transduction and activator of transcription 3 protect against cecal ligation and puncture-induced multiple organ damage and mortality. J Trauma. 2009;66:859–65.

    Article  Google Scholar 

  61. Li HY, Yao YM, Shi ZG, et al. Effect of 2,4-diamino-6-hydroxy-pyrimidine on postburn Staphylococcus aureus sepsis in rats. Crit Care Med. 2002;30:2520–7.

    Article  CAS  PubMed  Google Scholar 

  62. Chappell VL, Le LX, LaGrone L, et al. Stat proteins play a role in tumor necrosis factor alpha gene expression. Shock. 2000;14:400–2.

    Article  CAS  PubMed  Google Scholar 

  63. Yao S, Yao YM, Li HY, et al. The significance and potential role of signal transducers and activators of transcription 3 (STAT3) in postburn Staphylococcus aureus sepsis. Med J Chin PLA. 2002;27:763–6.

    CAS  Google Scholar 

  64. Yao S, Yao YM, Li HY, et al. The effect of inhibiting JAK/STAT pathway on acute liver injury in rats with postburn Staphylococcus aureus sepsis. Chin Crit Care Med. 2002;14:336–9.

    Google Scholar 

  65. Krebx DL, Hilton DJ. SOCS: physiological suppressors of cytokine signaling. J Cell Sci. 2000;113:2813–9.

    Google Scholar 

  66. Li HY, Yao YM, Dong N, et al. The significance of changes in suppressors of cytokine signaling in rats with postburn Staphylococcus aureus sepsis. Chin J Trauma. 2004;20:734–8.

    CAS  Google Scholar 

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Authors and Affiliations

  1. Burn Institute, First Hospital Affiliated to Chinese PLA General Hospital, Beijing, People’s Republic of China

    Yongming Yao (Prof.)

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  1. Yongming Yao
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  1. Third Military Medical University, Chongqing, Chong Qing, China

    Zongcheng Yang

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Yao, Y. (2015). Bacterial Endotoxin and Exotoxin in Severe Burns. In: Yang, Z. (eds) Chinese Burn Surgery. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-8575-4_5

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  • DOI: https://doi.org/10.1007/978-94-017-8575-4_5

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