软脑膜在外周炎症影响神经炎症过程中的作用
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摘要
阿尔茨海默病、帕金森病、额颞痴呆等慢性中枢神经退行性疾病的发病机制一直是学术界争论的热点问题。在这些疾病中,神经炎症是共有的特点。许多全身性疾病(如糖尿病、动脉粥样硬化及外周炎症)都与神经炎症的产生和加剧有关。越来越多的临床证据显示,一些常见的外周慢性炎症(如牙周炎等)与神经炎症的发生和发展有着密切的关系。近年来,一些学者的研究指出,软脑膜可能在这一相关性中起到了介导炎症信号传递的关键作用。本文就软脑膜在外周炎症影响神经炎症的过程中所起的作用进行综述,旨在进一步揭示神经炎症的病理过程,探究牙周炎和神经系统病变的内在联系,为众多慢性中枢神经退行性疾病的预防和治疗提供新途径。
The pathogenesis of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease dementia and frontotemporal dementia, has remained controversial in academic circles. However, the presence of neuroinflammation is a common feature in these neurodegenerative diseases. Moreover, systemic diseases, such as diabetes, atherosclerosis and peripheral inflammation, are associated with the occurrence and exacerbation of neuroinflammation. Many pieces of clinical evidence showed a correlation between some common kinds of chronic peripheral inflammation, for instance periodontitis, and neurodegenerative disease. To date, some studies indicated that leptomeninges possibly plays as the courier who transfers systemic inflammatory signals in this connection. This review retrospectively analysed the role of leptomeninges in this potential connection between peripheral inflammation neuroinflammation, described the pathological process of neuroinflammation and elucidated the relation between neurodegenerative diseases and paradentitis to develop new therapies and prevention of neurodegenerative diseases.
The pathogenesis of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease dementia and frontotemporal dementia, has remained controversial in academic circles. However, the presence of neuroinflammation is a common feature in these neurodegenerative diseases. Moreover, systemic diseases, such as diabetes, atherosclerosis and peripheral inflammation, are associated with the occurrence and exacerbation of neuroinflammation. Many pieces of clinical evidence showed a correlation between some common kinds of chronic peripheral inflammation, for instance periodontitis, and neurodegenerative disease. To date, some studies indicated that leptomeninges possibly plays as the courier who transfers systemic inflammatory signals in this connection. This review retrospectively analysed the role of leptomeninges in this potential connection between peripheral inflammation neuroinflammation, described the pathological process of neuroinflammation and elucidated the relation between neurodegenerative diseases and paradentitis to develop new therapies and prevention of neurodegenerative diseases.
引文
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[18]李卫,边艳青.外周炎症及慢性应激对认知功能的影响及影响机制[J].免疫学杂志,2014,30(7):650-653.Li W,Bian YQ.The effects of peripheral inflammation and chronic stress on cognitive function and its mechanisms[J].Immunol J,2014,30(7):650-653.
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[22]Berker E,Kantarci A,Hasturk H,et al.Blocking proinflammatory cytokine release modulates peripheral blood mononuclear cell response to Porphyromonas gingivalis[J].J Periodontol,2013,84(9):1337-1345.
[23]Foey AD,Crean S.Macrophage subset sensitivity to endotoxin tolerisation by Porphyromonas gingivalis[J].PLoS One,2013,8(7):e67955.
[24]Chen JH,Ke KF,Lu JH,et al.Protection of TGF-β1against neuroinflammation and neurodegeneration in Aβ1-42-induced Alzheimer’s disease model rats[J].PLoS One,2015,10(2):e0116549.
[25]Wu Z,Hayashi Y,Zhang J,et al.Involvement of prostaglandin E2 released from leptomeningeal cells in increased expression of transforming growth factor-beta in glial cells and cortical neurons during systemic inflammation[J].J Neurosci Res,2007,85(1):184-192.
[26]Skaper SD,Facci L,Giusti P.Mast cells,glia and neuroinflammation:partners in crime[J]Immunology,2014,141(3):314-327.
[27]Rodgers J,Bradley B,Kennedy PG,et al.Central nervous system parasitosis and neuroinflammation ameliorated by systemic IL-10 administration in trypanosoma brucei-infected mice[J].PLoS Negl Trop Dis,2015,9(10):e0004201.
[28]Hayder M,Varilh M,Turrin CO,et al.Phosphorusbased dendrimer ABP treats neuroinflammation by promoting IL-10-producing CD4+T Cells[J].Biomacromolecules,2015,16(11):3425-3433.
[29]Wilson KD,Stutz SJ,Ochoa LF,et al.Behavioural and neurological symptoms accompanied by cellular neuroinflammation in IL-10-deficient mice infected with Plasmodium chabaudi[J].Malar J,2016,15(1):428.
[30]Ruocco A,Nicole O,Docagne F,et al.A transforming growth factor-βantagonist unmasks the neuroprotective role of this endogenous cytokine in excitotoxic and ischemic brain injury[J].J Cereb Blood Flow Metab,1999,19(12):1345-1353.
[31]Wu Z,Tokuda Y,Zhang XW,et al.Age-dependent responses of glial cells and leptomeninges during systemic inflammation[J].Neurobiol Dis,2008,32(3):543-551.
[2]Liu X,Nemeth DP,Tarr AJ,et al.Euflammation attenuates peripheral inflammation-induced neuroinflammation and mitigates immune-to-brain signaling[J].Brain Behav Immun,2016,54:140-148.
[3]Huang L,Li X,Roberts J,et al.Differential role of P-glycoprotein and breast cancer resistance protein in drug distribution into brain,CSF and peripheral nerve tissues in rats[J].Xenobiotica,2015,45(6):547-555.
[4]Decimo I,Fumagalli G,Berton V,et al.Meninges:from protective membrane to stem cell niche[J].Am J Stem Cells,2012,1(2):92-105.
[5]Yasuda K,Cline C,Vogel P,et al.Drug transporters on arachnoid barrier cells contribute to the bloodcerebrospinal fluid barrier[J].Drug Metab Dispos,2013,41(4):923-931.
[6]Stolp HB,Liddelow SA,Sá-Pereira I,et al.Immune responses at brain barriers and implications for brain development and neurological function in later life[J].Front Integr Neurosci,2013,7:61.
[7]Wang T,Wang BR,Zhao HZ,et al.Lipopolysaccharide up-regulates IL-6R alpha expression in cultured leptomeningeal cells via activation of ERK1/2 pathway[J].Neurochem Res,2008,33(9):1901-1910.
[8]Liddelow SA,Dziegielewska KM,Ek CJ,et al.Correction:mechanisms that determine the internal environment of the developing brain:a transcriptomic,functional and ultrastructural approach[J].PLoSOne,2016,11(1):e0147680.
[9]Pasqualetti G,Brooks DJ,Edison P.The role of neuroinflammation in dementias[J].Curr Neurol Neurosci Rep,2015,15(4):17.
[10]Kranjac D,McLinden KA,Deodati LE,et al.Peripheral bacterial endotoxin administration triggers both memory consolidation and reconsolidation deficits in mice[J].Brain Behav Immun,2012,26(1):109-121.
[11]Semmler A,Frisch C,Debeir T,et al.Long-term cognitive impairment,neuronal loss and reduced cortical cholinergic innervation after recovery from sepsis in a rodent model[J].Exp Neurol,2007,204(2):733-740.
[12]Shi FD.Neuroinflammation[J].Neurosci Bull,2015,31(6):714-716.
[13]Muldoon LL,Alvarez JI,Begley DJ,et al.Immunologic privilege in the central nervous system and the bloodbrain barrier[J].J Cereb Blood Flow Metab,2013,33(1):13-21.
[14]Br?chner CB,Holst CB,M?llg?rd K.Outer brain barriers in rat and human development[J].Front Neurosci,2015,9:75.
[15]Wu Z,Nakanishi H.Connection between periodontitis and Alzheimer’s disease:possible roles of microglia and leptomeningeal cells[J].J Pharmacol Sci,2014,126(1):8-13.
[16]Dai L,DeFee MR,Cao Y,et al.Lipoteichoic acid(LTA)and lipopolysaccharides(LPS)from periodontal pathogenic bacteria facilitate oncogenic herpesvirus infection within primary oral cells[J].PLoSOne,2014,9(6):e101326.
[17]辛颖,胡月,唐琪,等.病原体相关分子模式与牙周炎的关系[J].华西口腔医学杂志,2016,34(1):96-99.Xin Y,Hu Y,Tang Q,et al.Correlation between pathogen-associated molecular patterns and periodontitis[J].West Chin J Stomatol,2016,34(1):96-99.
[18]李卫,边艳青.外周炎症及慢性应激对认知功能的影响及影响机制[J].免疫学杂志,2014,30(7):650-653.Li W,Bian YQ.The effects of peripheral inflammation and chronic stress on cognitive function and its mechanisms[J].Immunol J,2014,30(7):650-653.
[19]Singhrao SK,Harding A,Simmons T,et al.Oral inflammation,tooth loss,risk factors,and association with progression of Alzheimer’s disease[J].J Alzheimer’s Dis,2014,42:723-737.
[20]Wu Z,Zhang J,Nakanishi H.Leptomeningeal cells activate microglia and astrocytes to induce IL-10production by releasing pro-inflammatory cytokines during systemic inflammation[J].J Neuroimmunol,2005,167(1/2):90-98.
[21]Liu Y,Wu Z,Zhang X,et al.Leptomeningeal cells transduce peripheral macrophages inflammatory signal to microglia in reponse to Porphyromonas gingivalis LPS[J].Mediators Inflamm,2013,2013:407562.
[22]Berker E,Kantarci A,Hasturk H,et al.Blocking proinflammatory cytokine release modulates peripheral blood mononuclear cell response to Porphyromonas gingivalis[J].J Periodontol,2013,84(9):1337-1345.
[23]Foey AD,Crean S.Macrophage subset sensitivity to endotoxin tolerisation by Porphyromonas gingivalis[J].PLoS One,2013,8(7):e67955.
[24]Chen JH,Ke KF,Lu JH,et al.Protection of TGF-β1against neuroinflammation and neurodegeneration in Aβ1-42-induced Alzheimer’s disease model rats[J].PLoS One,2015,10(2):e0116549.
[25]Wu Z,Hayashi Y,Zhang J,et al.Involvement of prostaglandin E2 released from leptomeningeal cells in increased expression of transforming growth factor-beta in glial cells and cortical neurons during systemic inflammation[J].J Neurosci Res,2007,85(1):184-192.
[26]Skaper SD,Facci L,Giusti P.Mast cells,glia and neuroinflammation:partners in crime[J]Immunology,2014,141(3):314-327.
[27]Rodgers J,Bradley B,Kennedy PG,et al.Central nervous system parasitosis and neuroinflammation ameliorated by systemic IL-10 administration in trypanosoma brucei-infected mice[J].PLoS Negl Trop Dis,2015,9(10):e0004201.
[28]Hayder M,Varilh M,Turrin CO,et al.Phosphorusbased dendrimer ABP treats neuroinflammation by promoting IL-10-producing CD4+T Cells[J].Biomacromolecules,2015,16(11):3425-3433.
[29]Wilson KD,Stutz SJ,Ochoa LF,et al.Behavioural and neurological symptoms accompanied by cellular neuroinflammation in IL-10-deficient mice infected with Plasmodium chabaudi[J].Malar J,2016,15(1):428.
[30]Ruocco A,Nicole O,Docagne F,et al.A transforming growth factor-βantagonist unmasks the neuroprotective role of this endogenous cytokine in excitotoxic and ischemic brain injury[J].J Cereb Blood Flow Metab,1999,19(12):1345-1353.
[31]Wu Z,Tokuda Y,Zhang XW,et al.Age-dependent responses of glial cells and leptomeninges during systemic inflammation[J].Neurobiol Dis,2008,32(3):543-551.
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