Immunopathogenenis of sepsis

1. Martin, G. S., Mannino, D. M., Eaton, S., Moss, M. The epidemiology of sepsis in the United States from 1979 through 2000. N. England J. M., 2003, 348, p. 1546–1554.

2. Černý, V., Novák, I., Šrámek, V. Prevalence těžké sepse v České republice – prospektivní multicentrická jednodenní studie. Anest. intenziv. Med., 2003, 14, p. 218–222.

3. Angus, D. C., Linde-Zwirble, W. T., Lidicker, J. et al. Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care. Crit. Care Med., 2001, 29, p. 1303–1310.

4. Dombrovskiy, V. Y., Martin, A. A., Sunderram, J. et al. Rapid increase in hospitalization and mortality rates for severe sepsis in the United States: A trend analysis from 1993 to 2003. Crit. Care Med., 2007, 35, p. 1244–1250.

5. Dellinger, R. P. Cardiovascular management of septic shock. Crit. Care Med., 2003, 31, 3, p. 946–955.

6. Esper, A., Martin, G. S. Is severe sepsis increasing in incidence AND severity? Crit. Care Med., 2007, 35, 5, p. 1414–1415.

7. Bone, R. C., Balk, R. A.,Cerra, F. B. et al. American College of Chest Physicians/Society of Critical Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of Innovative therapies in sepsis. Chest, 1992, 101, p. 1644–1655.

8. Levy, M. M., Fink, M. P., Marshall, J. C. et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Intensive Care Med., 2003, 29, p. 530–538.

9. Calandra, T., Baumgartner, J. D., Grau, G. et al. Prognostic value of tumor necrosis factor/cachectin, interleukin-1, interferon-α, and interferon-γ in the serum of patients with septic shock. J. Infect. Dis., 1990, 161, p. 982–987.

10. Cassatella, M. A., Meda, L., Bonora, S. et al. Interleukin-10 (IL-10) inhibits the release of proinflammatory cytokines from human polymorphonuclear leukocytes. Evidence for an autocrine role of tumor necrosis factor and IL-1β in mediating the production of IL-8 triggered by lipopolysaccharide. J. Exp. Med., 1993, 178, p. 2207–2211.

11. Damas, P., Reuter, A., Gysen, P. et al. Tumor necrosis factor and interleukin-1 serum levels during severe sepsis in humans. Crit. Care Med., 1989, 17, p. 975–978.

12. Emery, P., Salmon, M. The immune response: systemic mediators of inflammation. Br. J. Hosp. Med., 1991, 45, 1, p. 64–168.

13. Abbas, A. K., Murphy, K. M., Sher, A. Functional diversity of helper T lymphocytes. Nature, 1996, 383, p. 787–793.

14. Borowikova, L. V., Ivanova, S., Zhang, H. et al. Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin. Nature, 2000, 405, p. 458–462.

15. Woiciechowsky, C., Asadullah, K., Nestler, D. et al. Sympathetic activation triggers systemic IL-10 release in immunodepression induced by brain injury. Nat. Med., 1998, 4, p. 808–813.

16. Heidecke, C. D., Hensler, T., Weighradt, H. et al. Selective defects of T lymphocytes function in patiens with lethal intraabdominal infection. Am. J. Surg., 1999, 178, p. 288–292.

17. Pellegrini, J. D., De Ak, J., Kodys, K. et al. Relationships between T lymphocytes apoptosis and anergy following trauma. J. Surg. Res., 2000, 88, p. 200–206.

18. Hotchkiss, R. S., Tinsley, K. W., Swanson, P. E. et al. Sepsis-induced apoptosis cause progressive profound depletion of B and CD4+ T lymphocytes in humans. J. Immunol., 2001, 166, p. 6952–6963.

19. Hotchkiss, R. S., Tinsley, K. W., Swanson, P. E. et al. Depletion of dendritic cells, but not macrophages, in patiens with sepsis. J. Immunol., 2002, 168, p. 2493–2500.

20. Fukuzuka, K., Edwards, C. K., Clare-Walter, M. et al. Glucocorticoid-induced, caspase – dependent organ apoptosis early after burn injury. Am. J. Physiol. Regul. Integr. Comp. Physiol., 2000, 278, p. R1005–1018.

21. Greene, D. R., Beere, H. M. Apoptosis:gone but not forgotten. Nature, 2000, 405, p. 28–29.

22. Fadok, V. A., Bratton, D. L., Rose, D. M. et al. A receptor for phosphatidylserine-specific clearence of apoptotic cells. Nature, 2000, 405, p. 85.

23. Eichacker, P. Q., Parent, C., Kalil, A. et al. Risk and the efficacy of antiinflammatory agents: retrospective and confirmatory studies of sepsis. Am. J. Respir. Crit. Care Med., 2002, 166, p. 1197–205.

24. Macias, W. L., Nelson, D. R., Wiliams, M. et al. Lack of evidence for qualitative treatment by disease severity interactions in clinical studies of severe sepsis. Crit. Care, 2005, 9, R607–622.

25. Marshall, J. C. The staging of sepsis: understanding heterogeneity in treatment efficacy. Crit. Care, 2005, 9, p. 626–628.

26. Průcha, M., Herold, I., Zazula, R., Dubská, L., Kavka, B. Monocytární deaktivace a produkce tumor nekrotizujícího faktoru-α ex vivo – prognostické parametry u pacientů jednotek intenzivní péče. Anest. intenziv. Med., 2003, 5, p. 223–228.

27. Calandra, T., Echtenacher, B., Le Roy, D. et al. Protection from septic shock by neutralization of macrophage migration inhibitory factor. Nature Medicine, 2000, 6, p. 164–170.

28. Wang, H., Zhang, M. et al. HMG-I as a late mediator of endotoxin letality in mice. Science, 1999, 285, p. 248–251.

29. Tschaikowsky, K., Geissing, M. H., Schiele, A. et al. Coincidence of pro- and anti-inflammatory responses in the early phase of severe sepsis: Longitudinal study of mononuclear histocompatibility leukocyte antigen – DR expression, procalcitonin, C-reactive protein, and changes in T-cell subsets in septic and postoperative patients. Crit. Care Med., 2002, 30, p. 1015–1023.

30. Oberholzer, A., Sousa, S. M., Tschoeke, S. K. et al. Plasma cytokine measurements augment prognostic scores as indicators of outcome in patients with severe sepsis. Shock, 2005, 23, p. 488–493.

31. Groeneveld, A. B. J., Bossink, A. W. J., Mierlo, G. J., Hack, C. E. Circulating inflammatory mediators in patients with fever: predicting bloodstream infection. Clin. Diagn. Lab. Immunology, 2001, 8, p. 1189–1195.

32. D’Andrea, A., Aste-Amezaga, M., Valiante, N. M. et al. Interleukin 10 (IL-10) inhibits human lymphocyte interferon gamma production by supressing natural killer cell stimulatory factor/IL-12 synthesis in accessory cells. J. Exp. Med., 1993, 178, p. 1041–1048.

33. De Vries, J. E., de Waal Malefyt K. Immunosuppressive and anti-inflammatory effects of human interleukin-10. In Faits, E., Baue, A. E., Schildberg, F. W. (Eds.) The immune consequences of trauma, shock and sepsis. Mechanisms and therapeutic approaches 1996. Pabst Science Publishers, p. 303–307.

34. Oberholzer, A., Oberholzer, C., Moldawer, L. L. Interleukin-10: a complex role in the pathogenesis of sepsis syndromes and its potential as an anti-inflammatory drug. Crit. Care Med., 2002, 30, S58–S63.

35. Janeway, C. A., Bottomly, K., Babich, J. Quantitative variation in Ia antigen expression plays a central role in immune regulation. Immunol. Today, 1984, 5, p. 99–105.

36. Docke, W. D., Syrbe, U., Meinecke, A. et al. Improvement of monocyte function – a new therapeutic approach? Update to Intensive Care and Emergency Medicine, 1994, 18, p. 473–500.

37. Rothe, G., Oser, A., Valet, G. Dihydrorhodamin 123: a new flow cytometric indicator for respiratory burst activity in neutrophil granulocytes. Naturwissenschaften, 1988, 73, p. 354–356.

38. Platzer, C., Richter, G., Uberla, K. et al. Analysis of cytokine mRNA levels in interleukin-4 transgenic mice by quantitative polymerase chain reaction. Eur. J. Immunol., 1992, 22, p. 1179–1184.

39. Munoz, C., Carlet, J., Fitting, C. et al. Dysregulation of in vitro cytokine production by monocytes during sepsis. J. Clin. Invest., 1991, 88, p. 1747–1754.

40. Abraham, E. Physiologic stress and cellular ischemia: Relationship immunosuppression and susceptibility to infection. Crit. Care Med., 1991, 19, p. 613–618.

41. Dinarello, C. A. The proinflammatory cytokine interleukin-1 and tumor necrosis factor and treatment of the septic shock syndrome. J. Infect. Dis., 1991, 163, p. 1177–1184.

42. Doughty, L., Patrene, K., Boggs, S. et al. Supression of native IL-10 production by constitutive expression of viral IL-10 (vIL-10) or soluble TNF receptor p75 (sTNFR) in mice. Abstr. Crit. Care Med., 1996, 24 (Suppl): A32.

43. Hamilton, G., Hofbauer, S., Hamilton, B. Endotoxin, TNF-α, interleukin-6 and parameters of the cellular immune system in patients with intraabdominal sepsis. Scand. J. Infect. Dis., 1992, 24, p. 361–368.

44. Cheadle, W. G., Hershman, M. J., Wellhausen, S. R. et al. Role of monocytic HLA-DR expression following trauma in predicting clinical outcome. In Faist, E., Ninnemann, J., Green, D. (Eds) Immune Consequences of Trauma, Shock and Sepsis. Springer-Verlag : Berlin, Heidelberg, New York 1989, p. 199–222.

45. De Waal Malefyt, K., Haanen, J., Spits, H. et al. Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen – specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class II major histocompatibility complex expression. J. Exp. Med., 1991, 174, p. 915–924.

46. Durez, P., Abramowicz, D., Gerard, C. et al. In vivo induction of interleukin 10 by anti- CD3 monoclonal antibody or bacterial lipopolysaccharide: differential modulation by cyclosporin. J. Exp. Med., 1993, 177, p. 551–555.

47. D’Andrea, A., Aste-Amezaga, M., Valiante, N. M. et al. Interleukin 10 (IL-10) inhibits human lymphocyte interferon gamma production by supressing natural killer cell stimulatory factor/IL-12 synthesis in accessory cells. J. Exp. Med., 1993, 178, p. 1041–1048.

48. De Vries, J. E., de Waal Malefyt, K. Immunosuppressive and anti-inflammatory effects of human interleukin-10. In Faits, E., Baue, A. E., Schildberg, F. W. (Eds.) The immune consequences of trauma, shock and sepsis. Mechanisms and therapeutic approaches 1996. Pabst Science Publishers, p. 303–307.

49. Chandry, D., Turner, M., Abney, A. et al. Modulation of cytokine production by transforming growth factor β. J. Immunol., 1989, 140, p. 4217–4222.

50. Espenik, T., Figari, I. S., Shalaby, M. R. et al. Inhibition of cytokine production by cyclosporin A and transforming growth factor β. J. Exp. Med., 1987, 166, p. 571–576.

51. Czarniecki, C. W., Chiu, H. H., Wong, G. H.W. et al. Transforming growth factor β modulates the expression of class II histocompatibility antigens on human cells. J. Immunol., 1988, 140, p. 4217–4222.

52. Oczenski, W., Krenn, H., Jilch, R. et al. HLA-DR as a marker for increased risk for systemic inflammation and septic complications after cardiac surgery. Intensive Care Med., 2003, dx.doi.org/10.1007/s00134-003-1826-8.

53. Perry, S. E., Modrala, S. M., Wenstone, R. et al. Is low monocyte HLA-DR expression helpful to predict outcome in severe sepsis? Intensive Care Med., 2003, dx.doi.org/10.1007/s00134-003-1686-2.

54. Braude, A. E., Jones, J. L., Douglas, H. The behavior of Escherichia coli endotoxin (somatic antigen) during infectious arthritis. J. Immunol., 1963, 90, p. 297– 301.

55. Andriole, V. T. Urinary tract infections in the 90s: Pathogenesis and management. Infection, 1992, 20 (suppl. 4), S251–S256,

56. Feltis, B. A., Jechorek, R. P., Erlanden, S. L. et al. Bacterial translocation and lipopolysaccharide – induced mortality in genetically macrophage-deficient op/op mice. Shock, 1994, 2, p. 29–33.

57. Go, L. L., Healey, P. J., Watkins, S. C. et al. The effect of endotoxin on intestinal mucosal permeability to bacteria in vitro. Arch. Surg., 1995, 130, p. 53–58.

58. Sedman, P. C., MacFie, J., Sagar, P. et al. The prevalence of gut translocation in humans. Gastroenterology, 1994, 107, p. 643–649.

59. Cabie, A., Farkas, J. C., Fitting, C. et al. High levels of portal TNF-α during abdominal aortic surgery in man. Cytokine, 1993, 5, p. 448–453.

60. Owens, W. E., Berg, R. D. Bacterial translocation from the gastrointestinal tract of thymectomized mice. Curr. Microbiol., 1982, 7, p. 169–174.

61. O’Boyle, C. J., Mac Fie, J., Mitchell, C. J. et al. Microbiology of bacterial translocation in humans. Gut, 1998, 42, p. 29–35.

62. Morin, M., Schindler, R., Wakabayashi, G. et al. Picogram concentrations of endotoxin stimulate synthesis of IL-1b and TNF-α by human peripheral blood mononuclear cells exposed to recombinant human C5a. Eur. Cytokine Netw., 1991, 2, p. 27–30.

63. Quereshi, S. T., Lariviere, G., Leveque, S. et al. Endotoxin-tolerant mice have mutations in Toll-like receptor 4. J. Exp. Med., 1999, 189, p. 615–625.

64. Cleveland, M. G., Gorham, J. D., Murphy, T. L. et al. Lipoteichoic acid preparations of Gram-positive bacteria induce interleukin-12 through a CD14 – dependent pathway. Infect. Immun., 1996, 64, p. 1906–1912.

65. Nwariaku, F., Sikes, P., Lightfoot, E. et al. Role of CD14 in hemorrhagic shock-induced alterations of the monocyte tumor necrosis factor response to endotoxin. J. Trauma, 1996, 40, p. 564–567.

66. Medzhitov, R., Janeway, C. Innate immunity: the virtues of a nonclonal system of recognition. Cell, 1997, 91, p. 295–298.

67. Hemmi, H. A Toll-like receptor recognizes bacterial DNA. Nature, 2000, 408, p. 740–745.

68. Ozinsky, A. The repertoire for pattern recognition of pathogens by the innate immune system is defined by cooperation between Toll-like receptors. Proc. Natl. Acad. Sci. USA, 2000, 97, p. 13766–13771.

69. Wiel, E., Lebuffe, G., Vallet, B. Bacterial CpG DNA in septic shock. In Vincent, J. L. (Ed.) Yearbook of Intensive Care and Emergency Medicine. 2002, p. 388–398.

70. Schouten, M., Wiersinga, W. J., Levi, M., van der Poll Inflammation, endothelium, and coagulation in sepsis. J. Leukoc. Biol., 2008, 83, p. 536–545.

71. Stief, T. W., Ijagha, O., Weiste, B. et al. Analysis of hemostasis alterations in sepsis. Blood Coagul. Fibrinolysis, 2007, 18, p. 179–186.

72. Cohen, J., Cristofaro, P., Carlet, J., Opal, S. New method of classifying infections in critically ill patients. Crit. Care Med., 2004, 32, p. 1510–1526.

73. Warris, A., Verweij, P. E., Gaustad, P. et al. Various Filamentous fungi digger in thein ability to induce TNF-α and IL-6 release in human monocyte culture. Agents Chemother., 2000, 40, p. 373–375.

74. Opal, S. M., Gerber, G. E., La Rosa, S. P. et al. Systemic host response in severe sepsis analyzed by causative microorganism and treatment effects of drotrecogin alfa (activated). Clin. Infect. Diseases, 2003, 37, p. 50–58.

75. Damas, P., Reuter, A., Gysen, P. et al. Tumor necrosis factor and interleukin-1 serum levels during severe sepsis in humans. Crit. Care Med., 1989, 17, p. 975–978.

76. Borrelli, E. et al. Plasma concentrations of cytokines, their soluble receptors, and antioxidant vitamins can predict the development of multiple organ failure in patients at risk. Crit. Care Med., 1996, 24, p. 392–397.

77. Dadák, L., Šťouračová, M., Štětka, P. et al. Rozšířený imunologický profil v prvních dnech pobytu a prognóza nemocných dlouhodobě hospitalizovaných na JIP. Anest. intenziv. Med., 2007, 3, s. 164-170.

78. Abraham, E., Laterre, P. F., Garbino, J. et al. Lenercept (p55 tumor necrosis factor receptor fusion protein) in severe sepsis and early septic shock: a randomized, double blind, placebo-controlled multicenter phase III trial with 1 342 patients. Crit. Care Med., 2001, 29, p. 503–510.

79. Fisher, C. J. Jr et al. Treatment of septic shock with the tumor necrosis factor receptor-fusion protein. N. Engl. J. Med., 1996, 334, p. 1697–1702.

80. Echtenacher, B., Urbaschek, R., Weigl, K. et al. Treatment of experimental sepsis-induced immunoparalysis with TNF. Immunobiology, 2003, 208, p. 381–389.

81. Remick, D. G., Bolgos, G., Copeland, S., Siddiqui, J. Role of interleukin 6 in mortality from a physiological response to sepsis. Infection and Immunity, 2005, 73, p. 2751–2757.

82. Bianchi, M. E. DAMPS, PAMPs and alarmins: all we need to know about danger. J. Leuko. Biology, 2007, 81, p. 1–5.

83. Wiersinga, W. J., van der Poll, T. The Role of Toll-like Receptors in Sepsis. In Yearbook of Intensive and emergency medicine. Springer : Berlin, Heidelberg 2006, p. 3–13.

84. Poltorak, A., He, X., Smirnova, I. et al. Defective LPS signaling in C3H/HeJ and C57BL/10ScR mice: Mutation in TLR4 gene. Science, 1998, 282, p. 2085–2088.

85. Beutler, B. Science review: key inflammatory and stress pathways in critical illness – the central role of the Toll-like receptors. Crit. Care, 2003, 7, p. 39–46.

86. Smirnova, I., Mann, N., Dols, A. et al. Assay of locus-specific genetic load implicates rare Toll-like receptor 4 mutations in meningococcal susceptibility. Proc. Natl. Acad. Sci. USA, 2003, 100, p. 6075–680.

87. Ayala, A., Lomas, J. L., Grutkoski, P. S., Chung, C. S. Pathological aspects of apoptosis in severe sepsis and shock? Int. J. Biochem. & Cell Biol., 2003, 35, p. 715–720.

88. Chung, C. S., Chaudry, I. H., Ayala, A. The apoptotic response of the lymphoid immune system to trauma, shock and sepsis. In Vincent, J. L. (editor) Yearbook of Intensive Care and Emergency Medicine. Springer-Verlag : Berlin 2000. p. 27–40.

89. Hotchkiss, R. S., Swanson, P. E., Freeman, B. D., Tinsley, K. W., Cobb, J. P., Matuschak, G. M. et al. Apoptotic cell death in patients with sepsis, shock and multiple organ dysfunction. Crit. Care Med., 1999, 27, p. 1230–1251.

90. Hotchkiss, R. S., Swanson, P. E., Knudson, C. M., Chang, M. et al. Overexpression of Bcl-2 in transgenic mice decreases apoptosis and improves survival in sepsis. J. Immunol., 1999, 162, p. 4148–4156.

91. Vol, R. E., Hermann, M., Roth, E. A. et al. Immunosuppressive effects of apoptotic cells. Nature, 1997, 390, p. 350.

92. Fadok, V. A., Bratton, D. L., Rose, D. M. et al. A receptor for phosphatidy serine-specific clearence of apoptotic cells. Nature, 2000, 405, p. 485–490.

93. Braun, J. S., Novak, R., Herzog, K. H. et al. Neuroprotection by a caspase inhibitor in acute bacterial meningitis. Nat. Med., 1999, 5, p. 298.

94. Chung, C. H. S., Ying, X. X., Wang, W., Ayala, A. Is Fas ligand or endotoxin responsible for mucosal lymphocyte apoptosis in sepsis? Arch. Surg., 1998, 133, p. 1213–11215.

95. Hotchkiss, R. S., Swanson, P. E., Freeman, B. D. et al. Prevention of lymphocyte cell death in sepsis improves survival in mice. Proc. Natl. Acad. Sci. USA, 1999, 96, p. 14541–14546.

96. Giamarellos-Bourboulis, E. J., Routsi, Ch., Plachouras, D. et al. Early apoptosis of blood monocytes in the septic host: is it a mechanism of protection in the event of septic shock? Critical Care, 2006, 10R76 (doi 10.1186/cc4921).

97. Wesche-Soldato, D. E., Stan, R. Z., Chung, Ch. S., Ayala, A. The apoptotic pathway as a therapeutic target in sepsis. Curr. Drug Targets, 2007, 8, p. 493–500.

98. Tang, A. H., Brunn, G. J., Cascalho, M., Platt, J. L. Pivotal advance: endogenous pathway to SIRS, sepsis, and related conditions. J. Leukoc. Biol., 2007, 82, p. 282–285.

99. Liu, D., Lu, F., Qin. G. et al. C1 inhibitor – mediated protection from sepsis. J. Immunol., 2007, 179, p. 3966–3972.

100. Guo, R. F., Ward, P. A. C5a, a therapeutic target in sepsis. Recent Patents Anti-Infect. Drug Disc., 2006, 1, p. 57–65.

101. Werdan, K. Immunoglobulin treatment in sepsis – is the answer „no“? Crit. Care Med., 2006, 34, p. 1542–1544.

102. Ishii, K. J., Uematsu, S., Akira, S. Toll Gates for future immunotherapy. Curr. Pharm. Des., 2006, 120, p. 4135–4142.

103. Suntharalingam, G., Perry, M. R., Ward, S., Brett, S. J., Castello-Cortes, A., Brunner, M. D., Panoskaltsis, N. Cytokine storm in a phase 1 trial of the anti-CD28 monoclonal antibody TGN1412. N. Engl. J. Med., 2006, 355, 10, p. 1018–1028.

104. Nierhaus, A., Montag, B., Timmler, N. et al. Reversal of immunoparalysis by recombinant human granulocyte – macrophage colony stimulating factor in patients with severe sepsis. Intensive Care Med., 2003, (on-line, Springer-Verlag 2003, 10.1007/s00134-003-1666-6).

105. Flohe, S. B., Agrawal, H., Flohe, S. et al. Diversity of interferon gamma and granulocyte-macrophage colony-stimulating factor in restoring immune dysfunction of dendritic cells and macrophages during polymicrobial sepsis. Mol. Med., 2008, Feb 24 [Epub ahead of print].

106. Eichacker, P. Q., Natanson, C. Increasing evidence that the risks of rhAPC may outweigh its benefits. Intensive Care Med., 2007; 33 p. 396–399.