Abstract
All forms of severe insult to the body, from trauma, burns, sepsis, and pancreatitis are associated with the activation and systemic expression of host inflammatory pathways via stimulation of the host immune effector cells to synthesize and release potent mediators of cell inflammation [1], This generalized process is often referred to as the systemic inflammatory response syndrome(SIRS) [2] to identify the non-specific aspects of its expression. Although the initial mediators of this process are often cytokines produced specifically in response to a pro-inflammatory stimulus, subsequently a vast array of protein and lipid mediator species is expressed in a complex network that at present defies simple description [3, 4]. The initiating cytokine usually is tumor necrosis factor-α (TNF-α) which induces a generalized up-regulation of the inflammatory cascades through binding to specific cell membrane receptors on immune competent cells.
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References
Schlag G, Redl H (1996) Mediators of injury and inflammation. World J Surg 20:406–410
Bone RC (1996) Toward a theory regarding the pathogenesis of the systemic inflammatory response syndrome: what we do and do not know about cytokine regulation. Crit Care Med 24: 163–172
Marsh CB, Wewers MD (1996) The pathogenesis of sepsis. Factors that modulate the response to gram-negative bacterial infection. Clin Chest Med 17:183–197
Crowley SR (1996) The pathogenesis of septic shock. Heart Lung 25:124–134
Pinsky MR, Vincent JL, Deviere J et al (1993) Serum cytokine levels in human septic shock. Relation to multiple-system organ failure and mortality. Chest 103:565–575
Thijs LG, Hack CE (1995) Time course of cytokine levels in sepsis. Intensive Care Med 21 [Suppl 2]:S258–S263
Blackwell TS, Christman JW (1996) Sepsis and cytokines: current status. Br J Anaesth 77: 110–117
Goldie AS, Fearon KC, Ross JA et al (1995) Natural cytokine antagonists and endogenous anti-endotoxin core antibodies in sepsis syndrome. The Sepsis Intervention Group. JAMA 274:172–117
Vanderpoll T, Malefyt RD, Coyle SM, Lowry SF (1997) Anti-inflammatory cytokine responses during clinical sepsis and experimental endotoxemia. Sequential measurements of plasma soluble interleukin(IL)-l receptor type li, IL-10, and IL-13. J Infect Dis 175:118–122
Ertel W, Scholl FA, Trentz O (1996) The role of anti-inflammatory mediators for the control of systemic inflammation following severe injury. In: Faist E, Baue AE, Schildberg FW (eds) The immune consequences of trauma, shock, and sepsis. Mechanisms and therapeutic approaches. Pabst Science Publishers, Lengerich, pp 453–470
Cavaillon JM (1995) The nonspecific nature of endotoxin tolerance. Trends Microbiol 3: 320–324
Ziegler-Heitbrock HWL, Wedel A, Schraut W et al (1994) Tolerance to lipopolysaccharide involves mobilization of nuclear factor kB with predominance of p 50 homodimers. J Biol Chem 269:17001–17004
Larue KEA, McCall CE (1994) A liable transcriptional repressor modulates endotoxin tolerance. J Exp Med 180:2269–2275
Pinsky MR (1994) Clinical studies on cytokines in sepsis: role of serum cytokines in the development of multiple-systems organ failure. Nephrol Dial Transplant 9[Suppl 4]:94–98
Martich GD, Boujoukos AJ, Suffredini AF (1993) Response of man to endotoxin. Immunobiology 187:403–416
Boutten A, Dehoux MS, Seta N et al (1996) Compartmentalized IL-8 and elastase release within the human lung in unilateral pneumonia. Am J Respir Crit Care Med 153:336–342
Hauser CJ (1996) Regional macrophage activation after injury and the compartmentalization of inflammation in trauma. New Horiz 4:235–251
Rosenbloom AJ, Pinsky MR, Bryant JL et al (1995) Leukocyte activation in the peripheral blood of patients with cirrhosis of the liver and SIRS. Correlation with serum interleukin-6 levels and organ dysfunction. JAMA 274:58–65
Tschaikowsky K, Sittl R, Braun GG et al (1993) Increased fMet-Leu-Phe receptor expression and altered superoxide production of neutrophil granulocytes in septic and posttraumatic patients. J Clin Invest 72:18–25
Trautinger F, Hammerle AF, Poschl G, Micksche M (1991) Respiratory burst capability of polymorphonuclear neutrophils and TNF-alpha serum levels in relationship to the development of septic syndrome in critically ill patients. J Leukoc Biol 49:449–454
Wenisch C, Parschalk P, Hasenhundl M et al (1995) Polymorphonuclear leukocyte dysregula-tion in patients with gram-negative septicemia assessed by flow cytometry. Eur J Clin Invest 25:418–424
McCall CE, Grosso-Wilmoth LM, LaRue K et al (1993) Tolerance to endotoxin-induced expression of the interleukin-1 beta gene in blood neutrophils of humans with the sepsis syndrome. J Clin Invest 91:853–861
Vespasiano MC, Lewandoski JR, Zimmerman JJ (1993) Longitudinal analysis of neutrophil superoxide anion generation in patients with septic shock. Crit Care Med 21:666–672
Sorrell TC, Sztelma K, May GL (1994) Circulating polymorphonuclear leukocytes from patients with gram-negative bacteremia are not primed for enhanced production of leukotriene B4 or 5-hydroxyeicosatetraenoic acid. J Infect Dis 169:1151–2114
Nakae H, Endo S, Inada K et al (1996) Changes in adhesion molecule levels in sepsis. Res Commun Mol Pathol Pharmacol 91:329–338
Fasano MB, Cousart S, Neal S, McCall CE (1991) Increased expression of the interleukin 1 receptor on blood neutrophils of humans with the sepsis syndrome. J Clin Invest 88: 1452–2149
Brom J, Koller M, Schlüter B et al (1995) Expression of the adhesion molecule CD11b and polymerization of actin by polymorphonuclear granulocytes of patients endangered by sepsis. Burns 21:427–431
Ljunghusen O, Berg S, Hed J et al (1995) Transient endotoxemia during burn wound revision causes leukocyte beta 2 integrin up-regulation and cytokine release. Inflammation 19:457–468
Lin RY, Astiz ME, Saxon JC et al (1994) Relationships between plasma cytokine concentrations and leukocyte functional antigen expression in patients with sepsis. Crit Care Med 22:1595–1602
Lin RY, Astiz ME, Saxon JC, Rackow EC (1993) Altered leukocyte immunophenotypes in septic shock. Studies of HLA-DR, CD11b, CD14, and IL-2R expression. Chest 104:847–853
Rosenbloom AJ, Levann D, Ray B et al (1996) Density and avidity changes of Cd11b on circulating polymorphonuclear leukocytes(PMN) in systemic inflammatory response syndrome(SIRS). Am J Respir Crit Care Med 153(4):A123(abstract)
Polla BS, Jacquier-Sarlin MR, Kantengwa S et al (1996) TNF-α alters mitochondrial membrane potential in L929 but not in TNF-α-resistance L929.12 cells: relationship with the expression of stress proteins, annexin 1 and superoxide dismutase activity. Free Radic Res 25: 125–131
Munoz C, Carlet J, Fitting C et al (1991) Dysregulation of vitro cytokine production by monocytes during sepsis. J Clin Invest 88:1747–1754
Jaaettla M, Wising D (1993) Heat shock proteins protect cells from monocyte cytotoxicity: possible mechanism of self protection. J Exp Med 177:231–236
Bellmann K, Wenz A, Radons J et al (1995) Heat shock induces resistance in rat pancreatic islet cells against nitric oxide, oxygen radicals and streptozototocin toxicity in vitro. J Clin Invest 95:2840–2845
Malyshev IY, Malugin AV, Golubeva LY et al (1996) Nitric oxide donor induces HSP70 accumulation in the heart and in cultured cells. FEBS Lett 391:21–23
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Pinsky, M.R. (1999). From Cytokines through Immune Effector Cells to the Body. In: Baue, A.E., Berlot, G., Gullo, A., Vincent, JL. (eds) Sepsis and Organ Dysfunction. Springer, Milano. https://doi.org/10.1007/978-88-470-2248-5_15
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DOI: https://doi.org/10.1007/978-88-470-2248-5_15
Publisher Name: Springer, Milano
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