Abstract
Understanding of the importance of inflammation’s role in many neurologic disease pathogenesis has increased rapidly in recent years. Neuroinflammation has been viewed as the most common phenomenon observed in disorders of the central nervous system (CNS), either in the acute insult, like infection, trauma, and stroke, or in chronic neurodegenerative states like Alzheimer’s disease, Parkinson disease and multiple sclerosis [1]. This ‘neuroinflammation hypothesis’ furth challenged attempts to expand our understanding of neuronal injury and neurodegeneration because of the activation of brain cells to stress and insult, and targeting neuroinflammation and the major elements of the inflammatory response has become the most effective neuroprotective strategy [2].
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References
Griffin WS, Sheng JG, Royston MC, et al (1998) Glial-neuronal interactions in Alzheimer’s disease: the potential role of a “cytokine cycle” in disease progression. Brain Pathol 8: 65–72
Craft JM, Watterson DM, Van Eldik LJ (2005) Neuroinflammation: a potential therapeutic target. Expert Opin Ther Targets 9: 887–900
Gasque P, Pontaine M, Morgan BP (1995) Complement expression in human brain. J Immunol. 154: 4726–4733
Arumugam TV, Shiels IA, Woodruff TM, Granger DN, Taylor SM (2004) The role of the complement system in ischemia-reperfusion injury. Shock 5: 401–409
Bradt BM, Kolb WP, Cooper NR (1998) Complement dependent proinflammatory proteins of Alzheimer’s disease beta-peptide. J Exp Med 188: 431–438
Kulkarni AP, Kellaway LA, Lahiri DK, Kotwal GJ (2004) Neuroprotection from complement-mediated inflammatory damage. Ann NY Acad Sci 1035: 147–164
Jacob A, Hensley LK, Safratowich BD, Quigg RJ, Alexander JJ (2007) The role of complement cascade in endotoxin-induced septic encephalopathy. Lab Invest 87: 1186–1194
Arumugam TV, Tang SC, Lathia JD, et al (2007) Intravenous immunoglobulin (IVIG) protects the brain against experimental stroke by preventing complement-mediated neuronal cell death. Proc Natl Acad Sci USA 104: 14104–14109
Sewell DL, Nacewicz B, Liu F, et al (2004) Complement C3 and C5 play critical roles in traumatic brain cryoinjury: blocking effects on neutrophil extravasation by C5a receptor antagonist. J Neuroimmunol 155: 55–63
Flierl MA, Stahel PF, Rittirsch D, et al (2009) Inhibition of complement C5a prevents breakdown of the blood-brain barrier and pituitary dysfunction in experimental sepsis. Crit Care 13: R12
Sapir T, Shoenfeld Y (2005) Facing the enigma of immunomodulatory effects of intravenous immunoglobulin. Clin Rev Allergy Immunol 180: 9–16
Lapointe BM, Herx LM, Gill V, Metz LM, Kubes P (2004) IVIg therapy in brain inflammation: etiology dependent differential effects on leukocyte recruitment. Brain 127: 2649–2656
Esen F, Senturk E, Ergin Ozcan P, et al. (2010) Intravenous immunoglobulins prevent breakdown of the blood-brain barrier in experimental sepsis. Crit Care 14(Suppl 1): P24(abst)
Skaper SD (2007) The brain as a target for inflammatory processes and neuroprotective strategies. Ann NY Acad Sci 1122: 23–34
Tracy KJ (2002) The inflammatory reflex. Nature 420: 853–859
Sharshar T, Hopkinson NS, Orlikowski D, Annane D (2005) Science review: The brain in sepsis — culprit and victim. Crit Care 9: 37–44
Papadopoulos MC, Davies DC, Moss RF, Tighe D, Bennett ED (2000) Pathophysiology of septic encephalopathy: a review. Crit Care Med 28: 3019–3024
Papadopoulos MC, Lamb FJ, Moss RF, Davies DC, Tighe D, Bennett ED (1999) Faecal peritonitis causes edema and neuronal injury in pig cerebral cortex Clin Sci 96: 461–466
Alexander JJ, Anderson AJ, Barnum SR, Stevens B, Tenner AJ (2008) The complement cascade Yin-Yang in neuroinflammation — neuro-protection and-degeneration. J Neurochem 107: 1169–1187
Lossinsky AS, Shivers RR (2004) Structural pathways for macromolecular and cellular transport across the blood-brain barrier during inflammatory conditions Review Histol Histopathol 19: 535–564
Gaillard PJ, de Boer AB, Breimer DD (2003) Pharmacological investigations on LPSinduced permeability changes in the blood-brain barrier invitro. Microvasc Res 65: 24–31
Vaszelka S, Urbanyi Z, Pazmany T, et al (2005) Human serum amyloid P component attenuates the bacterial lipopolysaccaride-induced increase in blood brain barrier permeability in mice. Neurosci Lett 352: 57–60
Arumugam TV, Woodruff TM, Lathia JD, Selvaraj PK, Mattson MP, Taylor SM (2009) Neuroprotection in stroke by complement inhibition and immunoglobulin therapy. Neuroscience 158: 1074–1089
Misra N, Bayry J, Ephrem A, et al (2005)Intravenous immunoglobulin in neurological disorders: a mechanistic perspective. J Neurol 252: 11–16
Antel J, Bar-Or A (2006) Roles of immunoglobulins and B cells in multiple sclerosis: from pathogenesis to treatment. J Neuroimmunol 180: 3–8
Hughes RA, Comblath DR (2005) Guillain-Barre syndrome. Lancet 366: 1653–1666
Dodel RC, Du Y, Depboylu C, et al (2004) Intravenous immunoglobulins containing antibodies against beta-amyloid for the treatment of Alzheimer’s disease. J Neurol Neurosurg Psychiatry 75: 1472–1474
Gok B, Sciubba DM, Okutan O, et al (2009) Immunomodulation of acute experimental spinal cord injury with human immunoglobulin. J Clin Neurosci 16: 549–553
Arumugam TV, Selvaraj PK, Woodruff TM, Mattson MP (2008) Targeting ischemic brain injury with intravenous immunoglobulin. Expert Opin Ther Targets 12: 19–29
Negi VS, Elluru S, Sibéril S, et al (2007) Intravenous immunoglobulin: an update on the clinical use and mechanisms of action. J Clin Immunol 27: 233–245
Stangel M, Compston A (2001) Polyclonal immunoglobulins (IVIg) modulate nitric oxide production and microglial functions invitro via Fc receptors. J Neuroimmunol 112: 63–71
Prasad NK, Papoff G, Zeuner A, et al (1998) Therapeutic preparations of normal polyspecific IgG (IVIg) induce apoptosis in human lymphocytesa nd monocytes: a novel mechanism of action od IVIg involving the Fas apoptotic pathway. J Immunol 161: 3781–3790
Basta M, Van Goor F, Luccioli S, et al (2003) F(ab)-mediated neutralization of C3a and C5a anaphylatoxins: a novel effector function of immunoglobulins. Nature Med 4: 431–438
Crow AR, Song S, Semple JW, Freedman J, Lazarus AH (2007) A role for IL-1 Receptor antagonist or other cytokines in the acute therapeutic effects of IVIg? Blood 109: 155–158
Jonas E, Dwenger A, Jonas M. (1995) Chemiluminescence response and adherence of neutrophils to cultured endothelial cells - influence of immunoglobulin G. J Biolumin Chemilumin 10: 169–173
Toungouz M, Denys CH, De Groote D, Dupont E (1995) In vitro inhibition of tumor necrosis factor-alpha and interleukin — 6 production by intravenous immunoglobulins. Br J Haematol 89: 698–703
Basta M (2008) Ambivalent effects of immunoglobulins on the complement system: Activation versus inhibition. Mol Immunol 45: 4073–4079
Ballander BM, Singhrao SK, Ohlsson M, Mattsson P, Svensson M (2001) Complement activation in the human brain after traumatic brain injury. J Neurotrauma 18: 1295–1311
Kaczorowski SL, Schiding JK, Toth CA, Kochanek PM (1995) Effect of soluble complement receptor-1 on neutrophil accumulation after traumatic brain injury in rats. J Cereb Blood Flow Metab 15: 860–864
Arumugam TV, Magnus T, Woodruff TM, Proctor LM, Shiels IA, Taylor SM (2006) Complement mediators in ischemia-reperfusion injury. Clin Chim Acta 374: 33–45
Mocco J, Mack WJ, Ducruet AF, et al (2006) Complement component C3 mediates inflammatory injury following focal cerebral ischemia. Circ Res 99: 209–217
O’Barr SA, Caguioa J, Gruol D, et al (2001) Neuronal expression of a functional receptor for the C5a complement activation fragment. J Immunol 166: 4154–4162
Persson M, Pekna M, Hansson E, Ronback L (2009) The complement derived anaphylatoxin C5a increases microglial GLT-1 expession and glutamate uptake in a TNF-a independent manner. Eur J Neurosci 29: 267–274
Faustmann PM, Krause D, Dux R, Dermietzel R (1995) Morphological study in the early stages of complement C5a fragment-induced experimental meningitis: activation of macrophages and astrocytes. Acta Neuropathol 89: 239–247
Riedemann NC, Guo RF, Neff TA, et al (2002) Increased C5a receptor expression in sepsis. J Clin Invest 110: 101–108
Annane D (2009) Sepsis associated delirium: the pro and con of C5a blockade. Crit Care 13: 135
Rieben R, Roos A, Mulzert Y, Tinguely C, Gerritsen AF, Daha MR (1999) Immunoglobulin M-enriched human intravenous immunoglobulin prevents complement activation in-vitro and in-vivo in a rat model of acute inflammation. Blood 93: 942–951
Laupland KB, Kirkpatrick AW, Delaney A (2007) Polyclonal intravenous immunoglobulin for the treatment of severe sepsis and septic shock in critically ill adults: a systematic review and metaanalysis. Crit Care Med 35: 2689–2692
Mohr M, Englisch L, Roth A, Burchardi H, Zielmann S (1997) Effects of early treatment with immunoglobulin on critical illness polyneuropathy following multiple organ failure and gram-negative sepsis. Intensive Care Med 23: 1144–1149
Werdan K, Pilz G, Bujdoso O, et al (2007) Score-based immunoglobulin G therapy of patients with sepsis: the SBITS study. Crit Care Med 35: 2693–2701
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Esen, F. (2011). Neuroprotection in Sepsis by Complement Inhibition and Immunoglobulin Therapy. In: Vincent, JL. (eds) Annual Update in Intensive Care and Emergency Medicine 2011. Annual Update in Intensive Care and Emergency Medicine 2011, vol 1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18081-1_58
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DOI: https://doi.org/10.1007/978-3-642-18081-1_58
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