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Langenbeck's Archives of Surgery

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01.09.2007 | Overview

Immune response of severely injured patients – influence of surgical intervention and therapeutic impact

verfasst von: S. Flohé, S. B. Flohé, F. U. Schade, C. Waydhas

Erschienen in: Langenbeck's Archives of Surgery | Ausgabe 5/2007

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Abstract

Backround

Severe injury leads to a severe deterioration of the patients’ immune response. The changes of the immune response after severe injury include a broad range of immune functions and may result in a status of immunosuppression, which could favor infectious complications. Therefore, immunostimulating therapies have been introduced in the therapy for severely injured patients in clinical and experimental settings.

Objectives

The article summarizes actual immunomodulating approaches in the treatment of trauma patients and therapeutic strategies avoiding additional immune deteriorations.

Results

Examples for an immunostimulating approach in trauma patients are interferonγ and the granulocyte macrophage-colony-stimulating factor (GM-CSF), which are summarized in this review in detail. However, the effect of such an interference in the patients’ immune response with all its different cellular targets is not yet clearly understood, and most studies focus on the reaction of circulating monocytes. In addition, further immunomodulating strategies, including nutritional support, are addressed. However, clinically established therapeutic immunomodulating strategies in trauma care so far do not exist. The impact of the accidental and also an additional surgical trauma on the immune response has been clearly demonstrated. Therefore, the idea of a “damage control orthopedic surgery” (DCOS) is not only necessary to prevent further deterioration of the homeostasis of, e.g., the coagulating system, but is also desirable in terms of minimizing the burden on the immune system. In addition, also the timing of secondary surgical treatment in trauma patient care should include an evaluation of the immune response, although the most reliable markers still need to be identified.

Conclusion

Immunomodulating therapies in trauma patients exist on an experimental level with inconsistent results. The general management of trauma patients includes strategies that have been developed also on the basis of immunological considerations.

Cavaillon JM, Adrie C, Fitting C, Adib-Conquy M (2005) Reprogramming of circulatory cells in sepsis and SIRS. J Endotoxin Res 11:311–320PubMed

Schmand JF, Ayala A, Chaudry IH (1994) Effects of trauma, duration of hypotension, and resuscitation regimen on cellular immunity after hemorrhagic shock. Crit Care Med 22:1076–1083PubMedCrossRef

Zellweger R, Ayala A, DeMaso CM, Chaudry IH (1995) Trauma–hemorrhage causes prolonged depression in cellular immunity. Shock 4:149–153PubMed

Flohé S, Ackermann M, Reuter M, Nast-Kolb D, Schade FU (2000) Sublethal hemorrhagic shock reduces tumor necrosis factor-alpha-producing capacity in different cell compartments. Eur Cytokine Netw 11:420–426PubMed

Hassoun HT, Kone BC, Mercer DW, Moody FG, Weisbrodt NW, Moore FA (2001) Post-injury multiple organ failure: the role of the gut. Shock 15:1–10PubMed

Sori AJ, Rush BF Jr, Lysz TW, Smith S, Machiedo GW (1988) The gut as source of sepsis after hemorrhagic shock. Am J Surg 155:187–192PubMed

Moore FA et al (1991) Gut bacterial translocation via the portal vein: a clinical perspective with major torso trauma. J Trauma 31:629–636 discussion 636–638PubMedCrossRef

Rock KL, Hearn A, Chen CJ, Shi Y (2005) Natural endogenous adjuvants. Springer Semin Immunopathol 26:231–246PubMedCrossRef

Hashiguchi N et al (2001) Enhanced expression of heat shock proteins in activated polymorphonuclear leukocytes in patients with sepsis. J Trauma 51:1104–1109PubMed

10.

Pespeni M et al (2005) Serum levels of Hsp60 correlate with the development of acute lung injury after trauma. J Surg Res 126:41–47PubMedCrossRef

11.

Flohé SB, Bangen JM, Flohé S, Agrawal H, Bergmann K, Schade FU (2007) Origin of immunomodulation after soft tissue trauma: Potential involvement of extracellular Heat-Shock. Shock 27:494–502PubMedCrossRef

12.

Huber-Lang M et al (2006) Generation of C5a in the absence of C3: a new complement activation pathway. Nat Med 12:682–687PubMedCrossRef

13.

Nast-Kolb D et al (1997) Indicators of the posttraumatic inflammatory response correlate with organ failure in patients with multiple injuries. J Trauma 42:446–454 discussion 454–455PubMed

14.

Donnelly TJ et al (1994) Cytokine, complement, and endotoxin profiles associated with the development of the adult respiratory distress syndrome after severe injury. Crit Care Med 22:768–776PubMedCrossRef

15.

Gebhard F, Pfetsch H, Steinbach G, Strecker W, Kinzl L, Bruckner UB (2000) Is interleukin 6 an early marker of injury severity following major trauma in humans? Arch Surg 135:291–295PubMedCrossRef

16.

Martin C, Boisson C, Haccoun M, Thomachot L, Mege JL (1997) Patterns of cytokine evolution (tumor necrosis factor-alpha and interleukin-6) after septic shock, hemorrhagic shock, and severe trauma. Crit Care Med 25:1813–1819PubMedCrossRef

17.

Roumen RM et al (1993) Cytokine patterns in patients after major vascular surgery, hemorrhagic shock, and severe blunt trauma. Relation with subsequent adult respiratory distress syndrome and multiple organ failure. Ann Surg 218:769–776PubMedCrossRef

18.

Liener UC, Bruckner UB, Knoferl MW, Steinbach G, Kinzl L, Gebhard F (2002) Chemokine activation within 24 hours after blunt accident trauma. Shock 17:169–172PubMedCrossRef

19.

Armstrong L, Millar AB (1997) Relative production of tumour necrosis factor alpha and interleukin 10 in adult respiratory distress syndrome. Thorax 52:442–446PubMedCrossRef

20.

Antonelli M et al (1994) Leukotrienes and alpha tumor necrosis factor levels in the bronchoalveolar lavage fluid of patient at risk for the adult respiratory distress syndrome. Minerva Anestesiol 60:419–426PubMed

21.

Giannoudis PV, Smith MR, Evans RT, Bellamy MC, Guillou PJ (1998) Serum CRP and IL-6 levels after trauma. Not predictive of septic complications in 31 patients. Acta Orthop Scand 69:184–188PubMedCrossRef

22.

Pape HC et al (1999) Levels of antibodies to endotoxin and cytokine release in patients with severe trauma: does posttraumatic dysergy contribute to organ failure? J Trauma 46:907–913PubMed

23.

DiPiro JT, Howdieshell TR, Goddard JK, Callaway DB, Hamilton RG, Mansberger AR Jr (1995) Association of interleukin-4 plasma levels with traumatic injury and clinical course. Arch Surg 130:1159–1162 discussion 1162–1153PubMed

24.

Majetschak M, Boergermann J, Waydhas C, Obertacke U, Nast-Kolb D, Schade FU (2000) Whole blood tumor necrosis factor-alpha production and its relation to systemic concentrations of interleukin 4, interleukin 10, and transforming growth factor-beta1 in multiply injured blunt trauma victims. Crit Care Med 28:1847–1853PubMedCrossRef

25.

Sherry RM, Cue JI, Goddard JK, Parramore JB, DiPiro JT (1996) Interleukin-10 is associated with the development of sepsis in trauma patients. J Trauma 40:613–616 discussion 616–617PubMed

26.

Menges T et al (1999) Changes in blood lymphocyte populations after multiple trauma: association with posttraumatic complications. Crit Care Med 27:733–740PubMedCrossRef

27.

Neidhardt R et al (1997) Relationship of interleukin-10 plasma levels to severity of injury and clinical outcome in injured patients. J Trauma 42:863–870 discussion 870–871PubMed

28.

Faist E et al (1987) Prostaglandin E2 (PGE2)-dependent suppression of interleukin alpha (IL-2) production in patients with major trauma. J Trauma 27:837–848PubMedCrossRef

29.

Miller-Graziano CL, Szabo G, Griffey K, Mehta B, Kodys K, Catalano D (1991) Role of elevated monocyte transforming growth factor beta (TGF beta) production in posttrauma immunosuppression. J Clin Immunol 11:95–102PubMedCrossRef

30.

Ditschkowski M et al (1999) HLA-DR expression and soluble HLA-DR levels in septic patients after trauma. Ann Surg 229:246–254PubMedCrossRef

31.

Livingston DH, Appel SH, Wellhausen SR, Sonnenfeld G, Polk HC Jr (1988) Depressed interferon gamma production and monocyte HLA-DR expression after severe injury. Arch Surg 123:1309–1312PubMed

32.

Ploder M et al (2006) Lipopolysaccharide-induced tumor necrosis factor alpha production and not monocyte human leukocyte antigen-DR expression is correlated with survival in septic trauma patients. Shock 25:129–134PubMed

33.

Keel M et al (1996) Different pattern of local and systemic release of proinflammatory and anti-inflammatory mediators in severely injured patients with chest trauma. J Trauma 40:907–912 discussion 912–914PubMed

34.

Ertel W et al (1995) Downregulation of proinflammatory cytokine release in whole blood from septic patients. Blood 85:1341–1347PubMed

35.

Marie C, Muret J, Fitting C, Losser MR, Payen D, Cavaillon JM (1998) Reduced ex vivo interleukin-8 production by neutrophils in septic and nonseptic systemic inflammatory response syndrome. Blood 91:3439–3446PubMed

36.

Majetschak M et al (1997) Regulation of whole blood tumor necrosis factor production upon endotoxin stimulation after severe blunt trauma. J Trauma 43:880–887PubMed

37.

Munoz C, Carlet J, Fitting C, Misset B, Bleriot JP, Cavaillon JM (1991) Dysregulation of in vitro cytokine production by monocytes during sepsis. J Clin Invest 88:1747–1754PubMed

38.

Williams MA et al (1998) Granulocyte-macrophage colony-stimulating factor induces activation and restores respiratory burst activity in monocytes from septic patients. J Infect Dis 177:107–115PubMedCrossRef

39.

Volk HD et al (1991) Alterations in function and phenotype of monocytes from patients with septic disease-predictive value and new therapeutic strategies. Behring Inst Mitt:208–215

40.

Volk HD et al (1996) Monocyte deactivation—rationale for a new therapeutic strategy in sepsis. Intensive Care Med 22 Suppl 4:S474–481PubMedCrossRef

41.

Lendemans S, Kreuzfelder E, Waydhas C, Nast-Kolb D, Flohé S (2004) Clinical course and prognostic significance of immunological and functional parameters after severe trauma. Unfallchirurg 107:203–210PubMedCrossRef

42.

Flohé SB, Agrawal H, Schmitz D, Gertz M, Flohé S, Schade FU (2006) Dendritic cells during polymicrobial sepsis rapidly mature but fail to initiate a protective Th1-type immune response. J Leukoc Biol 79:473–481PubMedCrossRef

43.

Hotchkiss RS et al (2002) Depletion of dendritic cells, but not macrophages, in patients with sepsis. J Immunol 168:2493–2500PubMed

44.

De AK, Laudanski K, Miller-Graziano CL (2003) Failure of monocytes of trauma patients to convert to immature dendritic cells is related to preferential macrophage-colony-stimulating factor-driven macrophage differentiation. J Immunol 170:6355–6362PubMed

45.

Meakins JL, McLean AP, Kelly R, Bubenik O, Pietsch JB, MacLean LD (1978) Delayed hypersensitivity and neutrophil chemotaxis: effect of trauma. J Trauma 18:240–247PubMed

46.

Christou NV et al (1995) The delayed hypersensitivity response and host resistance in surgical patients. 20 years later. Ann Surg 222:534–546; discussion 546–548PubMed

47.

Woltmann A, Kress HG (1991) The prognostic value of the delayed cutaneous immune reaction following multiple trauma in comparison with other clinical parameters. Anaesthesist 40:276–281PubMed

48.

Pape HC et al (2000) Biochemical changes after trauma and skeletal surgery of the lower extremity: quantification of the operative burden. Crit Care Med 28:3441–3448PubMedCrossRef

49.

Menger MD, Vollmar B (2004) Surgical trauma: hyperinflammation versus immunosuppression? Langenbecks Arch Surg 389:475–484PubMedCrossRef

50.

Asadullah K et al (1995) Immunodepression following neurosurgical procedures. Crit Care Med 23:1976–1983PubMedCrossRef

51.

Hiesmayr MJ et al (1999) Alterations in the number of circulating leucocytes, phenotype of monocyte and cytokine production in patients undergoing cardiothoracic surgery. Clin Exp Immunol 115:315–323PubMedCrossRef

52.

Decker D, Schondorf M, Bidlingmaier F, Hirner A, von Ruecker AA (1996) Surgical stress induces a shift in the type-1/type-2 T-helper cell balance, suggesting down-regulation of cell-mediated and up-regulation of antibody-mediated immunity commensurate to the trauma. Surgery 119:316–325PubMedCrossRef

53.

Mels AK et al (2001) Immune-stimulating effects of low-dose perioperative recombinant granulocyte-macrophage colony-stimulating factor in patients operated on for primary colorectal carcinoma. Br J Surg 88:539–544PubMedCrossRef

54.

Berger D, Bolke E, Seidelmann M, Beger HG (1997) Time-scale of interleukin-6, myeloid related proteins (MRP), C reactive protein (CRP), and endotoxin plasma levels during the postoperative acute phase reaction. Shock 7:422–426PubMedCrossRef

55.

Rotondo MF et al (1993) ‘Damage control’: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma 35:375–382 discussion 382–383PubMedCrossRef

56.

Harwood PJ, Giannoudis PV, van Griensven M, Krettek C, Pape HC (2005) Alterations in the systemic inflammatory response after early total care and damage control procedures for femoral shaft fracture in severely injured patients. J Trauma 58:446–452 discussion 452–454PubMed

57.

Pape HC et al (2003) Impact of intramedullary instrumentation versus damage control for femoral fractures on immunoinflammatory parameters: prospective randomized analysis by the EPOFF Study Group. J Trauma 55:7–13PubMed

58.

Pape H, Stalp M, v Griensven M, Weinberg A, Dahlweit M, Tscherne H (1999) Optimal timing for secondary surgery in polytrauma patients: an evaluation of 4,314 serious-injury cases. Chirurg 70:1287–1293PubMedCrossRef

59.

Waydhas C et al (1996) Posttraumatic inflammatory response, secondary operations, and late multiple organ failure. J Trauma 40:624–630 discussion 630–631PubMed

60.

Pape HC et al (2001) Major secondary surgery in blunt trauma patients and perioperative cytokine liberation: determination of the clinical relevance of biochemical markers. J Trauma 50:989–1000PubMed

61.

Flohé S, Lendemans S, Schade FU, Kreuzfelder E, Waydhas C (2004) Influence of surgical intervention in the immune response of severely injured patients. Intensive Care Med 30:96–102PubMedCrossRef

62.

Taeger G, Ruchholtz S, Waydhas C, Lewan U, Schmidt B, Nast-Kolb D (2005) Damage control orthopedics in patients with multiple injuries is effective, time saving, and safe. J Trauma 59:409–416 discussion 417PubMed

63.

Scalea TM, Boswell SA, Scott JD, Mitchell KA, Kramer ME, Pollak AN (2000) External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: damage control orthopedics. J Trauma 48:613–621 discussion 621–623PubMed

64.

Nowotarski PJ, Turen CH, Brumback RJ, Scarboro JM (2000) Conversion of external fixation to intramedullary nailing for fractures of the shaft of the femur in multiply injured patients. J Bone Joint Surg Am 82:781–788PubMedCrossRef

65.

Nast-Kolb D, Ruchholtz S, Waydhas C, Schmidt B, Taeger G (2005) Damage control orthopedics. Unfallchirurg 108(804):806–811

66.

Ertel W, Morrison MH, Ayala A, Dean RE, Chaudry IH (1992) Interferon-gamma attenuates hemorrhage-induced suppression of macrophage and splenocyte functions and decreases susceptibility to sepsis. Surgery 111:177–187PubMed

67.

Hershman MJ, Appel SH, Wellhausen SR, Sonnenfeld G, Polk HC, Jr (1989) Interferon-gamma treatment increases HLA-DR expression on monocytes in severely injured patients. Clin Exp Immunol 77:67–70PubMed

68.

Polk HC, Jr et al (1992) A randomized prospective clinical trial to determine the efficacy of interferon-gamma in severely injured patients. Am J Surg 163:191–196PubMedCrossRef

69.

Dries DJ et al (1994) Effect of interferon gamma on infection-related death in patients with severe injuries. A randomized, double-blind, placebo-controlled trial. Arch Surg 129:1031–1041 discussion 1042PubMed

70.

Turina M, Dickinson A, Gardner S, Polk HC, Jr (2006) Monocyte HLA-DR and interferon-gamma treatment in severely injured patients—a critical reappraisal more than a decade later. J Am Coll Surg 203:73–81PubMedCrossRef

71.

Hayes MP, Enterline JC, Gerrard TL, Zoon KC (1991) Regulation of interferon production by human monocytes: requirements for priming for lipopolysaccharide-induced production. J Leukoc Biol 50:176–181PubMed

72.

Lendemans S, Rani M, Selbach C, Kreuzfelder E, Schade FU, Flohé S (2006) GM-CSF priming of human monocytes is dependent on ERK1/2 activation. J Endotoxin Res 12:10–20PubMed

73.

Flohé S et al. (2003) Effect of granulocyte-macrophage colony-stimulating factor on the immune response of circulating monocytes after severe trauma. Crit Care Med 31:2462–2469PubMedCrossRef

74.

Fischer HG, Frosch S, Reske K, Reske-Kunz AB (1988) Granulocyte-macrophage colony-stimulating factor activates macrophages derived from bone marrow cultures to synthesis of MHC class II molecules and to augmented antigen presentation function. J Immunol 141:3882–3888PubMed

75.

Flohé S et al (1999) Influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) on whole blood endotoxin responsiveness following trauma, cardiopulmonary bypass, and severe sepsis. Shock 12:17–24PubMedCrossRef

76.

Bilgin K, Yaramis A, Haspolat K, Tas MA, Gunbey S, Derman O (2001) A randomized trial of granulocyte-macrophage colony-stimulating factor in neonates with sepsis and neutropenia. Pediatrics 107:36–41PubMedCrossRef

77.

Nierhaus A et al (2003) Reversal of immunoparalysis by recombinant human granulocyte-macrophage colony-stimulating factor in patients with severe sepsis. Intensive Care Med 29:646–651PubMed

78.

Wiltschke C, Krainer M, Nanut M, Wagner A, Linkesch W, Zielinski CC (1995) In vivo administration of granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor increases neutrophil oxidative burst activity. J Interferon Cytokine Res 15:249–253PubMedCrossRef

79.

Hartung T et al (1995) Effect of granulocyte colony-stimulating factor treatment on ex vivo blood cytokine response in human volunteers. Blood 85:2482–2489PubMed

80.

Schneider C, von Aulock S, Zedler S, Schinkel C, Hartung T, Faist E (2004) Perioperative recombinant human granulocyte colony-stimulating factor (Filgrastim) treatment prevents immunoinflammatory dysfunction associated with major surgery. Ann Surg 239:75–81PubMedCrossRef

81.

Schaefer H et al (2004) Perioperative granulocyte colony-stimulating factor does not prevent severe infections in patients undergoing esophagectomy for esophageal cancer: a randomized placebo-controlled clinical trial. Ann Surg 240:68–75PubMedCrossRef

82.

Heard SO et al (1998) Effect of prophylactic administration of recombinant human granulocyte colony-stimulating factor (filgrastim) on the frequency of nosocomial infections in patients with acute traumatic brain injury or cerebral hemorrhage. The Filgrastim Study Group. Crit Care Med 26:748–754PubMedCrossRef

83.

Jeschke MG, Herndon DN (2004) Effect of growth factors as therapeutic drugs on hepatic metabolism during the systemic inflammatory response syndrome. Curr Drug Metab 5:399–413PubMedCrossRef

84.

Fukushima R et al (1999) Prophylactic treatment with growth hormone and insulin-like growth factor I improve systemic bacterial clearance and survival in a murine model of burn-induced gut-derived sepsis. Burns 25:425–430PubMedCrossRef

85.

Huang Y, Wang SR, Yi C, Ying MY, Lin Y, Zhi MH (2002) Effects of recombinant human growth hormone on rat septic shock with intraabdominal infection by E. coli. World J Gastroenterol 8:1134–1137PubMed

86.

Takala J et al (1999) Increased mortality associated with growth hormone treatment in critically ill adults. N Engl J Med 341:785–792PubMedCrossRef

87.

Wu JC, Livingston DH, Hauser CJ, Deitch EA, Rameshwar P (2001) Trauma inhibits erythroid burst-forming unit and granulocyte-monocyte colony-forming unit growth through the production of TGF-beta1 by bone marrow stroma. Ann Surg 234:224–232PubMedCrossRef

88.

Choudhry MA, Bland KI, Chaudry IH (2006) Gender and susceptibility to sepsis following trauma. Endocr Metab Immune Disord Drug Targets 6:127–135PubMed

89.

Oberbeck R et al (2002) The effect of dehydroepiandrosterone on hemorrhage-induced suppression of cellular immune function. Intensive Care Med 28:963–968PubMedCrossRef

90.

Oberbeck R et al (2001) Dehydroepiandrosterone decreases mortality rate and improves cellular immune function during polymicrobial sepsis. Crit Care Med 29:380–384PubMedCrossRef

91.

Frantz MC et al. (2005) Dehydroepiandrosterone restores depressed peripheral blood mononuclear cell function following major abdominal surgery via the estrogen receptors. Crit Care Med 33:1779–1786PubMedCrossRef

92.

Boelens PG et al (2002) Glutamine-enriched enteral nutrition increases HLA-DR expression on monocytes of trauma patients. J Nutr 132:2580–2586PubMed

93.

Bastian L, Weimann A (2002) Immunonutrition in patients after multiple trauma. Br J Nutr 87 Suppl 1:S133–S134PubMedCrossRef

94.

Kotzampassi K, Giamarellos-Bourboulis EJ, Voudouris A, Kazamias P, Eleftheriadis E (2006) Benefits of a synbiotic formula (Synbiotic 2000Forte) in critically ill trauma patients: early results of a randomized controlled trial. World J Surg 30:1848–1855PubMedCrossRef

95.

Rayes N, Seehofer D, Muller AR, Hansen S, Bengmark S, Neuhaus P (2002) Influence of probiotics and fibre on the incidence of bacterial infections following major abdominal surgery—results of a prospective trial. Z Gastroenterol 40:869–876PubMedCrossRef

96.

Sugawara G et al (2006) Perioperative synbiotic treatment to prevent postoperative infectious complications in biliary cancer surgery: a randomized controlled trial. Ann Surg 244:706–714PubMedCrossRef

97.

Wasmuth HE et al (2004) Hyperglycemia at admission to the intensive care unit is associated with elevated serum concentrations of interleukin-6 and reduced ex vivo secretion of tumor necrosis factor-alpha. Crit Care Med 32:1109–1114PubMedCrossRef

98.

Oberbeck R (2006) Catecholamines: physiological immunomodulators during health and illness. Curr Med Chem 13:1979–1989PubMedCrossRef

99.

Keh D et al (2003) Immunologic and hemodynamic effects of “low-dose” hydrocortisone in septic shock: a double-blind, randomized, placebo-controlled, crossover study. Am J Respir Crit Care Med 167:512–520PubMedCrossRef

Titel: Immune response of severely injured patients – influence of surgical intervention and therapeutic impact
verfasst von: S. Flohé
S. B. Flohé
F. U. Schade
C. Waydhas
Publikationsdatum: 01.09.2007
Verlag: Springer-Verlag
Erschienen in: Langenbeck's Archives of Surgery / Ausgabe 5/2007
Print ISSN: 1435-2443
Elektronische ISSN: 1435-2451
DOI: https://doi.org/10.1007/s00423-007-0203-4

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Abstract

Backround

Objectives

Results

Conclusion

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