Neuroinflammation in ischemic stroke

ZHI Nan, XU Qun

Journal of Neurology and Neurorehabilitation ›› 2016, Vol. 12 ›› Issue (1) : 41-46.

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Journal of Neurology and Neurorehabilitation ›› 2016, Vol. 12 ›› Issue (1) : 41-46. DOI: 10.12022/jnnr.2016-0010
Review

Neuroinflammation in ischemic stroke

  • ZHI Nan, XU Qun
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Abstract

Neuroinflammation plays an important role in pathological injury after ischemic stroke. Increasing evidence suggests that neuroinflammation is a double-edged sword, as it not only exacerbates secondary brain injury in the acute stage of stroke, but also beneficially contributes to brain recovery after stroke. This paper reviews the key factors involved in neuroinflammation after ischemic stroke, including inflammatory cells, inflammatory mediators and adhesion molecules, describing their possible detrimental and protective effects in stroke. This review also briefly introduces recently studies about the advances and future perspectives in neuroinflammation after ischemic stroke.

Key words

Stroke / Neuroinflammation / Inflammatory cells / Inflammatory mediators

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ZHI Nan, XU Qun. Neuroinflammation in ischemic stroke[J]. Journal of Neurology and Neurorehabilitation. 2016, 12(1): 41-46 https://doi.org/10.12022/jnnr.2016-0010

References

[1] CHAMORRO A, HALLENBECK J. The harms and benefits of inflammatory and immune responses in vascular disease[J]. Stroke, 2006, 37(2):291-293.
[2] SAMSON Y, LAPERGUE B, HOSSEINI H. Inflammation and ischemic stroke: current status and future perspectives[J]. Rev Neurol (Paris), 2005, 161(12 Pt 1):1177-1182.
[3] BECKER K J. Targeting the central nervous system infammatory response in ischemic stroke[J]. Curr Opin Neurol, 2001, 14(3):349-353.
[4] LAKHAN S E, KIRCHGESSNER A, HOFER M. Inflammatory mechanisms in ischemic stroke: therapeutic approaches[J]. J Transl Med, 2009, 97(7):773.
[5] YILMAZ G, GRANGER D N. Cell adhesion molecules and ischemic stroke[J]. Neurol Res, 2008, 30(8):783-793.
[6] KRIZ J. Inflammation in ischemic brain injury: timing is important[J]. Crit Rev Neurobiol, 2006, 18(1-2):145-157.
[7] SCHILLING M, BESSELMANN M, LEONHAR C, et al. Microglial activation precedes and predominates over macrophage infiltration in transient focal cerebral ischemia: a study in green fluorescent protein transgenic bone marrow chimeric mice[J]. Exp Neurol, 2003, 183(1): 25-33.
[8] GERHARD A, NEUMAIER B, ELITOK E, et al. In vivo imaging of activated microglia using [11C]PK11195 and positron emission tomography in patients after ischemic stroke[J]. Neuroreport, 2000, 11(13):2957-2960.
[9] BUCK B H, LIEBESKIND D S, SAVER J L, et al. Early neutrophilia is associated with volume of ischemic tissue in acute stroke[J]. Stroke, 2008, 39(2): 355-360.
[10] KAUSHAL V, SCHLICHTER L C. Mechanisms of microglia-mediated neurotoxicity in a new model of the stroke penumbra[J]. Neurosci, 2008, 28(9):2221-2230.
[11] LEHNARDT S, MASSILLON L, FOLLETT P, et al. Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway[J]. Proc Natl Acad Sci U S A, 2003, 100(14):8514-8519.
[12] GÜNTHER A, KÜPPERS-TIEDT L, SCHNEIDER P M, et al. Reduced infarct volume and differential effects on glial cell activation after hyperbaric oxygen treatment in rat permanent focal cerebral ischemia[J]. Eur J Neurosci, 2005, 21(11):3189-3194.
[13] LAI A Y, TODD K G. Microglia in cerebral ischemia: molecular actions and interactions[J]. Can J Physiol Pharmacol, 2006, 84(1):49-59.
[14] ZHENG Z, YENARI M A. Post-ischemic inflammation: molecular mechanisms and therapeutic implications[J]. Neurol Res, 2004, 26(8):884-892.
[15] NADAREISHVILI Z G, LI H, WRIGHT V, et al. Elevated proinflammatory CD4+CD28- lymphocytes and stroke recurence and death[J]. Neurology, 2004, 63(8):1446-1451.
[16] DONG Y, BENVENISTE E N. Immune function of astrocytes[J]. Glia, 2001, 36(2):180-190.
[17] PEKNY M, NILSSON M. Astrocyte activation and reactive gliosis[J]. Glia, 2005, 50(4):427-434.
[18] AHMAD M, DAR N J, BHAT Z S, et al. Inflammation in ischemic stroke: mechanisms, consequences and possible drug targets[J]. CNS Neurol Disord Drug Targets, 2014, 13(8):1378-1396.
[19] KADHIM HJ, DUCHATEAU J, SÉBIRE G. Cytokines and brain injury: invited review[J]. J Intensive Care Med, 2008, 23(4):236-249.
[20] SIMI A, TSAKIRI N, WANG P, et al. Interleukin-1 and inflammatory neurodegeneration[J]. Biochem Soc Trans, 2007, 35 (Pt 5):1122-1126.
[21] WILDE G J, PRINGLE A K, SUNDSTROM L E, et al. Attenuation and augmentation of ischaemia-related neuronal death by tumour necrosis factor-alpha in vitro[J]. Eur J Neurosci, 2000, 12(11):3863-3870.
[22] SRIRAM K, O’CALLAGHAN J P. Divergent roles for tumor necrosis factor-alph in the brain[J]. J Neuroimmune Pharmacol, 2007, 2(2):140-153.
[23] HUANG J, UPADHYAY U M, TAMARGO R J. Inflammation in stroke and focal cerebral ischemia[J]. Surg Neurol, 2006, 66(3):232-245.
[24] CLARK W M, RINKER L G, LESSOV N S, et al. Lack of interleukin-6 expression is not prot-ective agains focal central nervous system ischemia[J]. Stroke, 2000, 31(7):1715-1720.
[25] EMSLEY H C, TYRRELL P J. Inflammation and infection in clinical stroke[J]. Cereb Blood Flow Metab, 2002, 22(12):1399-1419.
[26] SANCHEZ-MORENO C, DASHE J F, SCOTT T, et al. Decreased levels of plasma vitamin C and increased concentrations of inflammatory and oxidative stress markers after stroke[J]. Stroke, 2004, 35(1):163-168.
[27] COUGHLAN T, GIBSON C, MURPHY S. Modulatory effects of progesteroneon inducible nitric oxide synthase expression in vivo and in vitro[J]. J Neurochem, 2005, 93(4):932-942.
[28] PARK E M, CHO S, FRYS K A, et al. Inducible nitric oxide synthase contributes to gender differences in ischemic brain injury[J]. J Cereb Blood Flow Metab, 2006, 26(3):392-401.
[29] CHAN P H. Reactive oxygen radicals in signaling and damage in the ischemic brain[J]. J Cereb Blood Flow Metab, 2001, 21(1):2-14.
[30] HUANG J, CHOUDHRI T F, WINFREE C J, et al. Postischemic cerebrovascular E-selectin expression mediates tissue injuryin murine stroke[J]. Stroke, 2000, 31(12):3047-3053.
[31] BOWES MP, ZIVIN JA, ROTHLEIN R. Monoclonal antibody to the ICAM-1 adhesion site reduces neurological damage in a rabbit cerebral embolism stroke model[J]. Exp Neurol, 1993, 119(2):215-219.
[32] CONNOLLY E S JR, WINFREE C J, SPRINGER T A, et al. Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion. Role of neutrophil adhesion in the pathogenesis of stroke[J]. Clin Invest, 1996, 97(1):209-216.
[33] CHEN H, CHOPP M, ZHANG R L, et al. Anti-CD11b monoclonal antibody reduces ischemic cell damage after transient focal cerebral ischemia in rat[J]. Ann Neurol, 1994, 35(4):458-463.
[34] AHMAD M, GRAHAM S H. Inflammation after stroke: mechanisms and therapeutic approaches[J]. Transl Stroke Res, 2010, 1(2):74-84.
[35] DENES A, THORNTON P, ROTHWELL N J, et al. Inflammation and brain injury: Acute cerebral ischaemia, peripheral and central inflammation[J]. Brain Behav Immun, 2009, 24(5):708-723.
[36] EMSLEY H C, SMITH C J, GAVIN C M, et al. An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis[J]. J Neuroimmunol, 2003, 139(1-2):93-101.
[37] LAMPL Y, BOAZ M, GILAD R, et al. Minocycline treatment in acute stroke: an open-label, evaluator-blinded study[J]. Neurology, 2007, 69(14):1404-1410.
[38] ZHAO Y, REMPE D A. Targeting astrocytes for stroke therapy[J]. Neurotherapeutics, 2010, 7(4):439-451.
[39] BLOCK M L, ZECCA L, HONG J S. Microglia-mediated neurotoxicity: uncovering the molecular mechanisms[J]. Nat Rev Neurosci, 2007, 8(1):57-69.
[40] BASU A, LAZOVIC J, KRADY J K, et al. Interleukin-1 and the interleukin-1 type 1 receptor are essential for the progressive neurodegeneration that ensues subsequent to a mild hypoxic/ischemic injury[J]. J Cereb Blood Flow Metab, 2005, 25(1):17-29.
[41] LAZOVIC J, BASU A, LIN H W, et al. Neuroinflammation and both cytotoxic and vasogenic edema are reduced in interleukin-1 type 1 receptor-deficient mice conferring neuroprotection[J]. Stroke, 2005, 36(10):2226-2231.
[42] NAWASHIRO H, TASAKI K, RUETZLER C A, et al. TNF-alpha pretreatment induces protective effects against focal cerebral ischemia in mice[J]. J Cereb Blood Flow Metab, 1997, 17(5):483-490.
[43] ZHANG R L, CHOPP M, LI Y, et al. Anti-ICAM-1 antibody reduces ischemic cell damage after transient middle cerebral artery occlusion in the rat[J]. Neurology, 1994, 44(9):1747-1751.
[44] EMSLEY H C, SMITH C J, GEORGIOU R F, et al. A randomised phase II study of interleukin-1 receptor antagonist in acute stroke patients[J]. J Neurol Neurosurg Psychiatry, 2005, 76(10):1366-1372.
[45] KRAMS M, LEES K R, HACKE W, et al. Acute Stroke Therapy by Inhibition of Neutrophils (ASTIN): an adaptive dose-response study of UK-279,276 in acute ischemic stroke[J]. Stroke, 2003, 34(11):2543-2548.
[46] BECKER K J. Anti-leukocyte antibodies: LeukArrest (Hu23F2G) and Enlimomab (R6.5) in acute stroke[J]. Curr Med Res Opin, 2008(18 Suppl 2):s18-22.
[47] SMITH C J, DENES A, TYRRELL P J, et al. Phase II anti-inflammatory and immune-modulating drugs for acute ischaemic stroke[J]. Expert Opin Investig Drugs, 2015, 24(5):623-643.
[48] DZIEDZIC T. Clinical significance of acute phase reaction in stroke patients[J]. Front Biosci, 2008, 13(10):2922-2927.
[49] IDICULA T T, BROGGER J, NAESS H, et al. Admission C-reactive protein after acute ischemic stroke is associated with stroke severity and mortality: the ‘Bergen stroke study’[J]. BMC Neurol, 2009(9):18.
[50] PENNYPACKER K R. Targeting the peripheral inflammatory response to stroke: role of the spleen[J]. Transl Stroke Res, 2014, 5(6):635-637.
[51] OFFNER H, VANDENBARK A A, HURN P D. Effect of experimental stroke on peripheral immunity: CNS ischemia induces profound immunosuppression[J]. Neuroscience, 2009, 158(3):1098-1111.
[52] KLEHMET J, HARMS H, RICHTER M, et al. Stroke-induced immunodepression and post-stroke infections: lessons from the preventive antibacterial therapy in stroke trial[J]. Neuroscience, 2009, 158(3):1184-1193.
[53] DZIEDZIC T. Systemic inflammation as a therapeutic target in acute ischemic stroke[J]. Expert Rev Neurother, 2015, 15(5):523-531.

Funding

Shanghai Jiao Tong University Crossover Fund of Medicine, Engineering and Sciences (No. YG2012MS08)
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