Transfusion-induced immunomodulation and infectious complications

Česká verzia

Authors: M. Bucová ¹; M. Mistrík ²
Authors place of work: Imunologický ústav Lekárskej fakulty UK, Bratislava, Slovenská republika, prednosta prof. MUDr. Milan Buc, DrSc. ¹; Klinika hematológie a transfúziológie NsP sv. Cyrila a Metoda, Petržalka, Bratislava, Slovenská republika prednosta doc. MUDr. Martin Mistrík, CSc. ²
Published in the journal: Vnitř Lék 2006; 52(11): 1085-1092
Category: Review

Summary

Transfusions are not without risk. One of the side effects of transfusions is the development of transfusion-induced immunomodulation (TRIM) – primarily immunosuppression, but also a strong proinflammatory effect. This may be the cause of acute lung injury (TRALI), multiorgan failure (MOF), transfusion related acute-graft-versus-host-disease (TR AGvHD), as well as of the development of secondary nosocomial infections, mostly pulmonary infections, sepsis and wound infections, and also of elevated number of tumour relapses in oncological patients. The causes of TRIM development are the induction of microchimerism, different cells and also soluble factors – complement components, such as C3a, soluble HLA-I and HLA-II molecules (HLA – human leukocyte antigen), soluble Fas ligand (sFasL), and others. The immunosuppressive potential of blood products grows with the time of their storage and becomes highest in non-leukoreduced blood products stored for a long time. In view of possible adverse effects of a transfusion, the expected benefit should be balanced against possible risks.

Key words:
immunomodulation – immunosuppression – infection – microchimerism – transfusion – TRALI – TRIM

Zdroje

1. Fiebig EW, Busch MP. Emerging infections in transfusion medicine. Clin Lab Med 2004; 24: 797–823.

2. Offner PJ. Age of blood: does it make a difference? Crit Care 2004; 8: 24–26.

3. Dellinger EP, Anaya DA. Infectious and immunologic consequences of blood transfusion. Crit Care 2004; 8: 18–23.

4. Alter HJ. Transfusion transmitted hepatitis C and non-A, non-B, non-C virus infections. In: Simon T, Dzik W, Snyder E et al. Rossi’s principles of transfusion medicine. Philadelphia: Lippincott, Williams and Wilkins 2002: 718–732.

5. Bručkova M. Two decades of HIV/AIDS laboratory diagnosis in the Czech Republic. Epidemiol Microbiol Immunol 2004, 53: 162–164.

6. Dodd RY. Hepatitis A, hepatitis B, and non-A, non-B, non-C-viruses. In: Hillyer CD, Silberstein LE, Ness PM et al. Blood banking and transfusion medicine. Philadelphia: Churchill Livingstone 2003: 431–437.

7. Stanekova D. Aktuálne problémy základnej a nadstavbovej diagnostiky infekcie HIV. Slovenský lekár 2002; 3: 89–91.

8. Chiavetta JA, Escobar M, Newman A et al. Incidence and estimated rates of residual risk for HIV, hepatitis C, hepatitis B and human T-cell lymphotropic viruses in blood donors in Canada, 1990–2000. CMAJ 2003; 169: 767–773.

9. Goodnough LT Risks of blood transfusion. Anaesth Clin North America 2005; 23: 241–252.

10. Regan FAM, Hewitt P, Barbara JAJ et al. Prospective investigation of transfusion transmitted infection in recipients of over 20 000 units of blood. BMJ 2005; 320: 403–406.

11. Suchankova A, Stankova M, Roubalova K et al. Seroprevalence of HHV8 antibodies among the general population and HIV positive persons in the Czech Republic. J Clin Virol 2003; 28: 70–76.

12. Kuehnert MJ, Roth VR, Haley NR et al. Transfusion transmitted bacterial infection in the United States, 1998 through 2000. Transfusion 2001; 41: 1493–1499.

13. Krejsek J, Kopecký O Klinická imunologie. Nucleus, Hradec Králové 2004; 941.

14. Opelz G, Sengar DP, Mickey MR et al. Effect of blood transfusions on subsequent kidney transplants. Transplant Proc 1973; 5: 2353–259.

15. Opelz G, Vanrenterghem Y, Kirste G et al. Prospective evaluation of pretransplant blood transfusions in cadaver kidney recipients. Transplantation 1997; 63: 964–967.

16. Peters WR, Fry RD, Fleshman JW et al. Multiple blood transfusions reduce the recurrence rate of Crohn’s disease. Dis Colon Rectum 1989; 32: 749–753.

17. Unander AM. The role of immunization treatment in preventing recurrent abortion. Transfus Med Rev 1992; 6: 1–16.

18. Vamvakas E, Moore SB. Perioperative blood transfusion and colorectal cancer recurrence: a qualitative statistical overview and meta-analysis. Transfusion 1993; 33: 754–765.

19. Vignali A, Braga M, Gianotti L et al. A single unit of transfused allogeneic blood increases postoperative infections. Vox Sang 1996; 71: 170–175.

20. Ortolano AG, Russell R, Capetandes A et al. Transfusion associated immunosuppression – heuristic model or clinical concern. Mod Asp Immunobiol 2002; 2: 159–165.

21. Gianotti L, Pyles T, Alexander JW et al. Identification of the blood component responsible for increased susceptibility to gut-derived infection. Transfusion 1993; 33: 458–465.

22. Moore FA, Moore EE, Sauaia A. Blood transfusion. An independent risk factor for postinjury multiple organ failure. Arch Surg 1997; 132: 620–624.

23. Nagata S, Goldstein P. The Fas death factor. Science 1995; 267: 1449–1456.

24. Sauaia A, Moore FA, Moore EE et al. Early predictors of postinjury multiple organ failure. Arch Surg 1994; 129: 39–45.

25. Vamvakas EC, Carven JH. Transfusion and postoperative pneumonia in coronary artery bypass graft surgery: effect of the length of storage of transfused red cells. Transfusion 1999; 39: 701–710.

26. Vamvakas EC, Carven JH. RBC transfusion and postoperative length of stay in the hospital or the intensive care unit among patients undergoing coronary artery bypass graft surgery: the effects of confounding factors. Transfusion 2000; 40: 832–839.

27. Mincheff M. Changes in donor leukocytes during blood storage. Implications on post-transfusion immunomodulation and transfusion-associated GVHD. Vox Sang 1998; 74: 189–200.

28. Mincheff M, Loukinov D, Zoubak S et al. Fas and Fas ligand expression on human peripheral blood leukocytes. Vox Sang 1998; 74: 113–121.

29. Frabetti F, Tazzari PL, Mussiani D et al. White cell apoptosis in platelet concentrates. Transfusion 2000; 40: 160–168.

30. Bucová M. Sepsa – etiopatogenéza. Interná Med 2006; 6: 204–211.

31. Bucová M. Polarizácia lymfocytov T a úloha cytokínov v iniciálnom procese rozvoja autoimunity. Rheumatologia 2002; 16: 117–124.

32. Artlett CM. Pathophysiology of fetal microchimeric cells. Clin Chim Acta 2005; 360: 1–8.

33. Raghavan M, Marik PE. Anemia, allogenic blood transfusion, and immunomodulation in the critically ill. Chest 2005; 127: 295–307.

34. Ghio M, Contini P, Puppo F et al. The immunomodulatory effect of blood transfusions and intravenous immunoglobulins: the role of the soluble molecules of the Class–I major histocompatibility complex and of the Fas ligand. Ann Ital Med Int 2000; 15: 70–74.

35. Ghio M, Contini P, Mayyei C et al. In vitro immunosuppressive activity of soluble HLA class I and Fas ligand molecules: do they play a role in autologous blood transfusion? Transfusion 2001; 41: 988–996.

36. Puppo F, Ghio M, Contini P et al. Fas, Fas ligand, and transfusion immunomodulation. Transfusion 2001; 41: 416–418.

37. Goldsby RA, Kindt TJ, Osborne BA. Kuby Immunology. 4th ed. New York: Freeman WH and Company 2000: 351–370.

38. Adamashvili I, McVie R, Gelder F et al. Soluble HLA class I antigens in patients with type I Diabetes and their family members. Human Immunol 1997; 55: 176–183.

39. Matalliotakis IM, Athanassakis AG, Goumenou AG et al. The possible antiinflammatory role of circulating human leucocyte antigen levels in women with endometriosis after treatment with danazol and leuprozalin acetate depot. Mediators of Inflammation 2001; 10: 75–80.

40. Contini P, Ghio M, Merlo A et al. Apoptosis of antigen-specific T lymphocytes upon the engagement of CD8 by soluble HLA class I molecules is Fas ligand/ Fas mediated: evidence for the involvement of p56lck, calcium calmodulin kinase II, and Calcium-independent protein kinase C signaling pathways and for NF-kappaB and NF-AT nuclear translocation. J Immunol 2005; 1: 7244–7254.

41. Puppo F, Contini P, Ghio M et al. Soluble human MHC class I molecules induce soluble Fas ligand secretion and trigger apoptosis in activated CD8(+) Fas (CD95)(+) T lymphocytes. Int Immunol 2000; 12: 195–203.

42. Puppo F, Contini P, Ghio M et al. Soluble HLA class I molecules/CD8 ligation trigger apoptosis of CD8+ cells by Fas/Fas-ligand interaction. Scient World J 2002; 12: 421–423.

43. Kirkley SA. Proposed mechanisms of transfusion – induced immunomodulation. Clin Diag Lab Immunol 1999; 6: 652–657.

44. Mincheff MS, Meryman HT, Kapoor V et al. Blood transfusion and immunomodulation: a possible mechanism. Vox Sang 1993; 65: 18–24.

45. Contini P, Ghio M, Poggi A et al. Soluble HLA-A, -B, -C and -G molecules induce apoptosis in T and NK CD8+ cells and inhibit cytotoxic T cell activity through CD8 ligation. Eur J Immunol 2003; 33: 125–134.

46. Bucová M. Regulačné T–bunky a autoimunita. Rheumatologia 2002; 16: 189–193.

47. Bushell A, Karim M, Kingsley CI et al. Pretransplant blood transfusion without additional immunotherapy generates CD25+ CD4+ regulatory T cells: A potential explanation for the blood transfusion effect. Transplantation 2003; 76: 449–455.

48. Procházková R. Multikomponentné automatizované odbery – nový trend v dárcovství krve. Vnitř Lék 2005; 51: 320–326.