Abstract
The clinical syndrome referred to as “systemic inflammatory response” (SIRS) has long been recognized as a cascade of pro-inflammatory mediator activities that overcome compensatory anti-inflammatory activities. Moreover, the excessive activity of several immune cell mediators (cytokines), such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1), are believed to be responsible for the hemodynamic instability and manifestations of organ failure in critically ill patients [1, 2]. However, several clinical trials utilizing agents directed against these cytokines have demonstrated limited efficacy, with no significant reduction in the incidence of endorgan failure or mortality [3]. These clinical failures have prompted a reappraisal of the influences of pro-inflammatory mediators and the complexities of their contribution to the inflammatory process. Paramount to these efforts are investigations at the cellular level particularly as they pertain to receptor-signaling, functional integrity of immune cells during systemic insults (i.e. infectious, traumatic, thermal), and the mechanisms for homeostatic regulation of dysfunctional immunocytes.
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References
Van der Poll T, Lowry SF (1995) Endogenous mechanisms regulating TNF and IL-1 during sepsis. In: Vincent JL (ed) Yearbook of Intensive Care and Emergency Medicine 1995, pp 385–397
Guirao X, Lowry SF (1996) The biologic control of injury and inflammation: Much more than too little or too late. World J Surg 20: 437–446
Opal SM (1995) Clinical trials of novel therapeutic agents: Why did they fail? In: Vincent JL (ed) Yearbook of Intensive Care and Emergency Medicine 1995, pp 425–436
Kerr JF, Wyllie AH, Currie AR (1972) Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer 26: 239–257
Lee A, Whyte KB, Haslett C (1993) Inhibition of apoptosis and prolongation of neutrophil functional longevity by inflammatory mediators. J Leukocyte Biol 54: 283–288
Biffl WL, Moore EE, Moore FA, et al (1996) Interleukin-6 delays neutrophil apoptosis. Arch Surg 131: 24–30
Mangan DF, Wahl SM (1991) Differential regulation of human monocyte programmed cell death (apoptosis) by chemotactic factors and pro-inflammatory cytokines. J Immunol 147: 3408–3412
Rogy MA, Oldenburg HSA, Coyle S, Trousdale R, Moldawer LL, Lowry SF (1996) Correlation between acute physiology and chronic health evaluation (APACHE III score) and immunological parameters in critically ill patients with sepsis. Brit J Surg 83: 396–400
Agosti JM, Fisher JC, Opal SM, et al (1994) Treatment of patients with sepsis syndrome with solube TNF receptor (sTNFR). Antimicrob Agents Chemother 65: M3 (Abst)
Fisher DJ, Agosti JM, Opal SM, Lowry SF, et al (1996) Treatment of septic shock with the tumor necrosis factor receptor: Fc fusion protein. N Engl J Med 334: 1697–1702
Savill J, Dransfield I, Hogg N, Haslett C (1990) Vitronectin receptor-mediated phagocytosis of cells undergoing apoptosis. Nature 343: 170–176
Meagher LC, Savill JS, Baker A, et al (1992) Phagocytosis of apoptotic neutrophils does not induce macrophage release of thromboxane B2. J Leukocyte Biol 52: 269–273
Squier MKT, Sehnert AJ, Cohen JJ (1995) Apoptosis in leukocytes. J Leukocyte Biol 57: 2–10
Saville JS, Wyllie AH, Henson JE, et al (1989) Macrophage phagocytosis of aging neutrophils in inflammation: Programmed cell death in the neutrophil leads to its recognition by macrophages. J Clin Invest 83: 865–875
Van der Poll T, Lowry SF (1995) Tumor necrosis factor in sepsis: Mediator of multiple organ failure or essential part of host defense? Shock 3: 1–12
Bazzoni F, Beutler B (1996) The tumor necrosis factor ligand and receptor families. N Engl J Med 334: 1717–1725
Tartaglia LA, Goeddel DV (1992) Two TNF receptors. Immunol Today 13: 151–153
Jarvis WD, Kolesnick RN, Fornari FA, Traylor RS, Gewirtz DA, Grant S (1994) Induction of apoptotic DNA damage and cell death by activation of the sphingomyelin pathway. Proc Natl Acad Sci USA 91: 73–77
MacEwan DJ (1996) Elevated cPLA2 levels as a mechanism by which the p70 TNF and p75 NGF receptors enhance apoptosis. FEBS Letters 379: 77–81
Vandenabeele P, Declercq W, Vanhaesbroeck B, et al (1995) Both TNF receptors are required for TNF-mediated induction of apoptosis in PC60 cells. J Immunol 154: 2904–2913
Bigda J, Beletsky I, Brakebusch C, et al (1994) Dual role of the p75 tumor necrosis factor (TNF) receptor in TNF cytotoxicity. J Exp Med 180: 445–460
Suda T, Takahashi T, Golstein P, et al (1993) Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family. Cell 75: 1169–1178
Nagata S, Golstein P (1995) The Fas death factor. Science 267: 1449–1456
Fisher GH, Tosenberg FJ, Straus SE, et al (1995) Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome. Cell 81: 935–946
Boldin MP, Mett IL, Varfolomeev EE, et al (1995) Self-association of the “death domains” of the p55 tumor necrosis factor (TNF) receptor and Fas/APO1 prompts signaling of TNF and Fas/APO1 effects. J Biol Chem 20: 387–391
Chu K, Niu XH, Williams LT (1995) A Fas-associated protein factor, FAF1, potentiates Fas-mediated apoptosis. Proc Nat Acad Sci USA 92: 11 894–11 898
Obeid LM, Linardic CM, Karolak LA, Hannun YA (1993) Programmed cell death induced by ceramide. Science 259: 1769–1771
Kolesnick R, Golde DW (1994) The sphingomyelin pathway in tumor necrosis factor and interleukin-1 signaling. Cell 77: 325–328
Troiano L, Monti D, Cossarizza A, et al (1995) Involvement of CD45 in dexamethasone-and heat shock-induced apoptosis of rat thymocytes. Biochem Biophys Res Commun 214: 941–948
Blackwell TS, Blackwell TR, Holden EP, Christman BW, Christman JW (1996) In vivo antioxidant treatment suppresses nuclear factor-KB activation and neutrophilic lung inflammation. J Immunol 157:1630–1637
Siebenlist U, Granzoso G, Brown K (1994) Structure, regulation and function of NF-KB. Annu Rev Cell Biol 10: 405–412
Korsmeyer SJ (1992) Bd-2: An antidote to programmed cell death. Cancer Surveys 15:105–118
Memon SA, Moreno MB, Petrak D, Zacharchuk CM (1995) Bd-2 blocks glucocorticoid-but not Fas-or activation-induced apoptosis in a T cell hybridoma. J Immunol 155: 4644–4652
Bradbury D, Zhu YM, Russell N (1994) Regulation of bd-2 expression and apoptosis in acute myeloblastic leukemia cells by granulocyte-macrophage colony-stimulating factor. Leukemia 8: 776–779
Ivanov VN, Deng G, Podack ER, Malek TR (1995) Pleiotropic effects of bd-2 on transcription factors in T cells: Potential role of NF-x13 p50-p50 for the anti-apoptotic function of bd-2. Int Immunol 7: 1709–1720
Lagasse E, Weissman IL (1994) Bc1–2 inhibits apoptosis of neutrophils but not their engulfment by macrophages. J Exp Med 179: 1047–1052
Van der Poll T, Galvano SE, Kumar A, et al (1995) Endotoxin induces downregulation of tumor necrosis factor receptors on circulating monocytes and granulocytes in humans. Blood 86: 2754–2759
Calvano SE, van der Poll T, Coyle SM, et al (1996) Monocyte tumor necrosis factor receptor levels as a predictor of risk in human sepsis. Arch Surg 131: 434–437
Colotta F, Re F, Polentarutti N, Sozzani S, Mantovani A (1992) Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products. Blood 80: 2012–2020
Mangan DF, Welch GR, Wahl SM (1991) Lipopolysaccharide, tumor necrosis factor-a, and IL-lß prevent programmed cell death (apoptosis) in human peripheral blood monocytes. J Immunol 146: 1541–1546
Mangan DF, Robertson B, Wahl SM (1992) IL-4 enhances programmed cell death (apoptosis) in stimulated human monocytes. J Immunol 148: 1812–1816
Fleischmann J, Golde DW, Weisbart RH, Gasson JC (1986) Granulocyte-macrophage colony-stimulating factor enhances phagocytosis of bacteria by human neutrophils. Blood 68: 708–711
Lundblad R, Nesland JM, Giercksky KE (1996) Granulocyte colony-stimulating factor improves survival rate and reduces concentrations of bacteria, endotoxin, tumor necrosis factor, and endothelin-1 in fulminant intra-abdominal sepsis in rats. Grit Care Med 24: 820–826
Wing EJ, Magee DM, Whiteside TL, Kaplan SS, Shadduck RK (1989) Recombinant human granulocyte/macrophage colony-stimulating factor enhances monocyte cytotoxicity and secretion of tumor necrosis factor-a and interferon in cancer patients. Blood 73: 643–646
Williams MA, Kouroumoussis I, Syndercombe-Court D, et al (1995) Administration of recombinant human granulocyte-macrophage colony-stimulating factor after chemotherapy regulates the expression and secretion of monocyte tumor necrosis factor (TNF) and TNF receptors p55 and p75. Blood 86: 4234–4242
Bach MK, Brashler JR (1995) Evidence that granulocyte/macrophage-colony-stimulating factor and interferon-y maintain the viability of human peripheral blood monocytes in part by their suppression of IL-10 production. Int Arch Allergy Immunol 107: 90–92
Watson RWG, Rotstein OD, Nathens AB, Dackiw APB, Marshall JC (1996) Thiol-mediated redox regulation of neutrophil apoptosis. Surgery 120: 150–158
Meduri GU, Headley S, Kohler G, et al (1995) Persistent elevation of inflammatory cytokines predicts a poor outcome in ARDS. Chest 107: 1062–1073
Steinberg KP, Milberg JA, Martin TR, Maunder RJ, Cockrill BA, Hudson LD (1994) Evolution of bronchoalveolar cell populations in the adult respiratory distress syndrome. J Respir Crit Care Med 150: 113–122
Cox G, Crossley J, Xing Z (1995) Macrophage engulfment of apoptotic neutrophils contributes to the resolution of acute pulmonary inflammation in vivo. Am J Respir Cell Mol Biol 12: 232–237
Leist M, Gantner F, Bohlinger I, Tiegs G, Germann PG, Wendel A (1995) Tumor necrosis factor-induced hepatocyte apoptosis precedes liver failure in experimental murine shock models
Galle PR, Hofmann WJ, Walczak H (1995) Involvement of the CD95 (APO-1/Fas) receptor and ligand in liver damage J Exp Med 11: 1223–1230
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Lin, E., Calvano, S.E., Lowry, S.F. (1997). Disordered Apoptosis as a Mechanism for Adverse Outcome. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1997. Yearbook of Intensive Care and Emergency Medicine, vol 1997. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-13450-4_9
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DOI: https://doi.org/10.1007/978-3-662-13450-4_9
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