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Die klinische Relevanz von DAMP („damage-associated molecular pattern“) für den postoperativen Verlauf nach thorakoabdomineller Aortenchirurgie

Eine selektive Literaturrecherche

Clinical relevance of damage-associated molecular patterns (DAMP) for the postoperative course after thoracoabdominal aortic surgery

A selective literature search

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Literatur

  1. Coselli JS et al (2016) Outcomes of 3309 thoracoabdominal aortic aneurysm repairs. J Thorac Cardiovasc Surg 151(5):1323–1337

    PubMed  Google Scholar 

  2. Bone RC et al (1992) Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest 136(5 Suppl):e28–2009

    Google Scholar 

  3. Hoover L et al (2006) Systemic inflammatory response syndrome and nosocomial infection in trauma. J Trauma 61(2):310–316 (discussion 316–7)

    PubMed  Google Scholar 

  4. Hotchkiss RS, Monneret G, Payen D (2013) Immunosuppression in sepsis: a novel understanding of the disorder and a new therapeutic approach. Lancet Infect Dis 13(3):260–268

    CAS  PubMed  PubMed Central  Google Scholar 

  5. Bochicchio GV et al (2002) Persistent systemic inflammatory response syndrome is predictive of nosocomial infection in trauma. J Trauma 53(2):245–250 (discussion 250–1)

    PubMed  Google Scholar 

  6. Jacobs MJ et al (2007) Surgical repair of thoracoabdominal aortic aneurysms. J Cardiovasc Surg (torino) 48(1):49–58

    CAS  Google Scholar 

  7. Vourc’h M, Roquilly A, Asehnoune K (2018) Trauma-induced damage-associated molecular patterns-mediated remote organ injury and Immunosuppression in the acutely ill patient. Front Immunol 9:1330

    PubMed  PubMed Central  Google Scholar 

  8. Manson J, Thiemermann C, Brohi K (2012) Trauma alarmins as activators of damage-induced inflammation. Br J Surg 99(Suppl 1):12–20

    CAS  PubMed  Google Scholar 

  9. Ma KC et al (2018) The role of danger signals in the pathogenesis and perpetuation of critical illness. Am J Respir Crit Care Med 197(3):300–309

    CAS  PubMed  PubMed Central  Google Scholar 

  10. Zhang Q et al (2010) Circulating mitochondrial DAMPs cause inflammatory responses to injury. Nature 464(7285):104–107

    CAS  PubMed  PubMed Central  Google Scholar 

  11. Simmons JD et al (2013) Elevated levels of plasma mitochondrial DNA DAMPs are linked to clinical outcome in severely injured human subjects. Ann Surg 258(4):591–596 (discussion 596–8)

    PubMed  Google Scholar 

  12. Kariko K et al (2004) mRNA is an endogenous ligand for Toll-like receptor 3. J Biol Chem 279(13):12542–12550

    CAS  PubMed  Google Scholar 

  13. He ZW et al (2013) HMGB1 acts in synergy with lipopolysaccharide in activating rheumatoid synovial fibroblasts via p38 MAPK and NF-kappaB signaling pathways. Mediators Inflamm. https://doi.org/10.1155/2013/596716

    PubMed  PubMed Central  Google Scholar 

  14. Andrassy M et al (2008) High-mobility group box-1 in ischemia-reperfusion injury of the heart. Circulation 117(25):3216–3226

    CAS  PubMed  Google Scholar 

  15. Tsung A et al (2005) The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion. J Exp Med 201(7):1135–1143

    CAS  PubMed  PubMed Central  Google Scholar 

  16. Yang R et al (2006) Anti-HMGB1 neutralizing antibody ameliorates gut barrier dysfunction and improves survival after hemorrhagic shock. Mol Med 12(4–6):105–114

    CAS  PubMed  PubMed Central  Google Scholar 

  17. Cohen MJ et al (2009) Early release of high mobility group box nuclear protein 1 after severe trauma in humans: role of injury severity and tissue hypoperfusion. Crit Care 13(6):R174

    PubMed  PubMed Central  Google Scholar 

  18. Venereau E et al (2012) Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release. J Exp Med 209(9):1519–1528

    CAS  PubMed  PubMed Central  Google Scholar 

  19. Timmermans K et al (2016) Plasma levels of danger-associated molecular patterns are associated with immune suppression in trauma patients. Intensive Care Med 42(4):551–561

    CAS  PubMed  PubMed Central  Google Scholar 

  20. Pockley AG, Shepherd J, Corton JM (1998) Detection of heat shock protein 70 (Hsp70) and anti-Hsp70 antibodies in the serum of normal individuals. Immunol Invest 27(6):367–377

    CAS  PubMed  Google Scholar 

  21. Pittet JF et al (2002) Serum levels of Hsp 72 measured early after trauma correlate with survival. J Trauma 52(4):611–617 (discussion 617)

    PubMed  Google Scholar 

  22. Foell D et al (2007) S100 proteins expressed in phagocytes: a novel group of damage-associated molecular pattern molecules. J Leukoc Biol 81(1):28–37

    CAS  PubMed  Google Scholar 

  23. Roth J et al (1992) Complex pattern of the myelo-monocytic differentiation antigens MRP8 and MRP14 during chronic airway inflammation. Immunobiology 186(3–4):304–314

    CAS  PubMed  Google Scholar 

  24. Dar MI et al (2001) Single aortic cross-clamp technique reduces S‑100 release after coronary artery surgery. Ann Thorac Surg 71(3):794–796

    CAS  PubMed  Google Scholar 

  25. Vos PE et al (2010) GFAP and S100B are biomarkers of traumatic brain injury: an observational cohort study. Baillieres Clin Neurol 75(20):1786–1793

    CAS  Google Scholar 

  26. Schober A, Bernhagen J, Weber C (2008) Chemokine-like functions of MIF in atherosclerosis. J Mol Med 86(7):761–770

    CAS  PubMed  Google Scholar 

  27. Asare Y, Schmitt M, Bernhagen J (2013) The vascular biology of macrophage migration inhibitory factor (MIF). Expression and effects in inflammation, atherogenesis and angiogenesis. Thromb Haemost 109(3):391–398

    CAS  PubMed  Google Scholar 

  28. Payen D et al (2012) A multicentre study of acute kidney injury in severe sepsis and septic shock: association with inflammatory phenotype and HLA genotype. PLoS ONE 7(6):e35838

    CAS  PubMed  PubMed Central  Google Scholar 

  29. Stefaniak J et al (2015) Macrophage migration inhibitory factor as a potential predictor for requirement of renal replacement therapy after orthotopic liver transplantation. Liver Transpl 21(5):662–669

    PubMed  Google Scholar 

  30. Al-Abed Y et al (2005) ISO-1 binding to the tautomerase active site of MIF inhibits its pro-inflammatory activity and increases survival in severe sepsis. J Biol Chem 280(44):36541–36544

    CAS  PubMed  Google Scholar 

  31. Kleemann R et al (2000) Intracellular action of the cytokine MIF to modulate AP-1 activity and the cell cycle through Jab1. Nature 408(6809):211–216

    CAS  PubMed  Google Scholar 

  32. Gombert A et al (2017) Macrophage migration inhibitory factor predicts outcome in complex aortic surgery. Int J Mol Sci 18(11):2374

    PubMed Central  Google Scholar 

  33. Li J et al (2018) Blocking macrophage migration inhibitory factor protects against cisplatin-induced acute kidney injury in mice. Mol Ther 26(10):2523–2532

    CAS  PubMed  Google Scholar 

  34. Simon TP et al (2017) Plasma adrenomedullin in critically ill patients with sepsis after major surgery: a pilot study. J Crit Care 38:68–72

    CAS  PubMed  Google Scholar 

  35. Tolppanen H et al (2017) Adrenomedullin: a marker of impaired hemodynamics, organ dysfunction, and poor prognosis in cardiogenic shock. Ann Intensive Care 7(1):6

    PubMed  PubMed Central  Google Scholar 

  36. Hinrichs S et al (2018) P283The precursor Pro-Adrenomedullin is an active protein: it supports cardiomyocyte survival and regulates cardiac inflammation related to myocardial infarction. Cardiovasc Res 114(suppl_1):S73–S73

    Google Scholar 

  37. Kawai C et al (2016) Circulating extracellular histones are clinically relevant mediators of multiple organ injury. Am J Pathol 186(4):829–843

    CAS  PubMed  Google Scholar 

  38. Dear JW et al (2011) Cyclophilin A is a damage-associated molecular pattern molecule that mediates acetaminophen-induced liver injury. J Immunol 187(6):3347–3352

    CAS  PubMed  Google Scholar 

  39. Fiane AE et al (2003) Mechanism of complement activation and its role in the inflammatory response after thoracoabdominal aortic aneurysm repair. Circulation 108(7):849–856

    CAS  PubMed  Google Scholar 

  40. Welborn MB et al (2000) The relationship between visceral ischemia, proinflammatory cytokines, and organ injury in patients undergoing thoracoabdominal aortic aneurysm repair. Crit Care Med 28(9):3191–3197

    CAS  PubMed  Google Scholar 

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Correspondence to A. Gombert.

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A. Gombert, J. Grommes und M.J. Jacobs geben an, dass kein Interessenkonflikt besteht.

Dieser Beitrag beinhaltet keine von den Autoren durchgeführten Studien an Menschen oder Tieren.

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Gombert, A., Grommes, J. & Jacobs, M.J. Die klinische Relevanz von DAMP („damage-associated molecular pattern“) für den postoperativen Verlauf nach thorakoabdomineller Aortenchirurgie. Gefässchirurgie 24, 173–175 (2019). https://doi.org/10.1007/s00772-019-0510-4

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