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[PMID]:29238017
[Au] Autor:Nakane S; Mukaino A; Ando Y
[Ad] Endereço:Department of Neurology, Graduate School of Medical Sciences, Kumamoto University.
[Ti] Título:[The interface between the immune system and autonomic nervous system].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(5):352-360, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  The nervous system and the immune system are two major systems in human body. Although it was revealed these two systems correlated, the control of immune cell dynamics by the nervous system has come to draw a lot of attention at the present time. Recent advances in basic and preclinical science reveal that reflex neural circuits inhibit the production of cytokines and inflammation in several animal models. One well-characterized cytokine-inhibiting mechanism, termed the "inflammatory reflex", is dependent upon vagus nerve stimulation that inhibits cytokine production and attenuates the inflammation. And the mechanism for controlling lymphocyte trafficking becomes clear, and molecular basis of immune regulation by the nervous system was reported. On the other hand, the nervous system is protected from the invasion of harmful agents by the barrier. However, there are neuroimmunological disorders, which is associated with autoimmunity, tumor immunity, and infection immunity. Autoimmune autonomic ganglionopathy (AAG) is an acquired immune-mediated disorder that leads to widespread autonomic manifestations, in which autoantibodies to ganglionic nicotinic acetylcholine receptors play a central role. Previously, we elucidated the prevalence of extra-autonomic manifestations in patients with AAG. It is necessary to establish the new systems for the detection of autoantibodies to other subunits of acetylcholine receptor.
[Mh] Termos MeSH primário: Sistema Nervoso Autônomo/imunologia
Sistema Imunitário/imunologia
Inflamação/imunologia
[Mh] Termos MeSH secundário: Animais
Autoanticorpos/imunologia
Autoimunidade/imunologia
Citocinas/imunologia
Citocinas/metabolismo
Gânglios Autônomos/imunologia
Seres Humanos
Neuroimunomodulação/imunologia
Receptores Colinérgicos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Cytokines); 0 (Receptors, Cholinergic)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.352


  2 / 3264 MEDLINE  
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[PMID]:28970585
[Au] Autor:Okusa MD; Rosin DL; Tracey KJ
[Ad] Endereço:Division of Nephrology, Center for Immunity, Inflammation and Regenerative Medicine, PO Box 800133, 1300 Jefferson Park Avenue - West Complex, 5 th floor, Charlottesville, Virginia 22908-0133, USA.
[Ti] Título:Targeting neural reflex circuits in immunity to treat kidney disease.
[So] Source:Nat Rev Nephrol;13(11):669-680, 2017 Nov.
[Is] ISSN:1759-507X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neural pathways regulate immunity and inflammation via the inflammatory reflex and specific molecular targets can be modulated by stimulating neurons. Neuroimmunomodulation by nonpharmacological methods is emerging as a novel therapeutic strategy for inflammatory diseases, including kidney diseases and hypertension. Electrical stimulation of vagus neurons or treatment with pulsed ultrasound activates the cholinergic anti-inflammatory pathway (CAP) and protects mice from acute kidney injury (AKI). Direct innervation of the kidney, by afferent and efferent neurons, might have a role in modulating and responding to inflammation in various diseases, either locally or by providing feedback to regions of the central nervous system that are important in the inflammatory reflex pathway. Increased sympathetic drive to the kidney has a role in the pathogenesis of hypertension, and selective modulation of neuroimmune interactions in the kidney could potentially be more effective for lowering blood pressure and treating inflammatory kidney diseases than renal denervation. Use of optogenetic tools for selective stimulation of specific neurons has enabled the identification of neural circuits in the brain that modulate kidney function via activation of the CAP. In this Review we discuss evidence for a role of neural circuits in the control of renal inflammation as well as the therapeutic potential of targeting these circuits in the settings of AKI, kidney fibrosis and hypertension.
[Mh] Termos MeSH primário: Imunidade Inata
Nefropatias/terapia
Neuroimunomodulação
Reflexo/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Nefropatias/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1038/nrneph.2017.132


  3 / 3264 MEDLINE  
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[PMID]:28827386
[Au] Autor:Suvas S
[Ad] Endereço:Department of Ophthalmology/Kresge Eye Institute, Wayne State University School of Medicine, Detroit, MI 48201; ssuvas@med.wayne.edu.
[Ti] Título:Role of Substance P Neuropeptide in Inflammation, Wound Healing, and Tissue Homeostasis.
[So] Source:J Immunol;199(5):1543-1552, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Substance P (SP) is an undecapeptide present in the CNS and the peripheral nervous system. SP released from the peripheral nerves exerts its biological and immunological activity via high-affinity neurokinin 1 receptor (NK1R). SP is also produced by immune cells and acts as an autocrine or paracrine fashion to regulate the function of immune cells. In addition to its proinflammatory role, SP and its metabolites in combination with insulin-like growth factor-1 are shown to promote the corneal epithelial wound healing. Recently, we showed an altered ocular surface homeostasis in unmanipulated NK1R mice, suggesting the role of SP-NK1R signaling in ocular surface homeostasis under steady-state. This review summarizes the immunobiology of SP and its effect on immune cells and immunity to microbial infection. In addition, the effect of SP in inflammation, wound healing, and corneal epithelial homeostasis in the eye is discussed.
[Mh] Termos MeSH primário: Inflamação/imunologia
Sistema Nervoso
Neuroimunomodulação
Neurotransmissores/imunologia
Substância P/imunologia
[Mh] Termos MeSH secundário: Animais
Córnea/metabolismo
Córnea/patologia
Homeostase
Seres Humanos
Fator de Crescimento Insulin-Like I/análogos & derivados
Fator de Crescimento Insulin-Like I/metabolismo
Camundongos
Receptores da Neurocinina-1/genética
Receptores da Neurocinina-1/metabolismo
Transdução de Sinais
Cicatrização
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neurotransmitter Agents); 0 (Receptors, Neurokinin-1); 0 (insulin-like growth factor-1 D peptide); 33507-63-0 (Substance P); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601751


  4 / 3264 MEDLINE  
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[PMID]:28636961
[Au] Autor:Herz J; Filiano AJ; Smith A; Yogev N; Kipnis J
[Ad] Endereço:Center for Brain Immunology and Glia, Department of Neuroscience, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA.
[Ti] Título:Myeloid Cells in the Central Nervous System.
[So] Source:Immunity;46(6):943-956, 2017 Jun 20.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The central nervous system (CNS) and its meningeal coverings accommodate a diverse myeloid compartment that includes parenchymal microglia and perivascular macrophages, as well as choroid plexus and meningeal macrophages, dendritic cells, and granulocytes. These myeloid populations enjoy an intimate relationship with the CNS, where they play an essential role in both health and disease. Although the importance of these cells is clearly recognized, their exact function in the CNS continues to be explored. Here, we review the subsets of myeloid cells that inhabit the parenchyma, meninges, and choroid plexus and discuss their roles in CNS homeostasis. We also discuss the role of these cells in various neurological pathologies, such as autoimmunity, mechanical injury, neurodegeneration, and infection. We highlight the neuroprotective nature of certain myeloid cells by emphasizing their therapeutic potential for the treatment of neurological conditions.
[Mh] Termos MeSH primário: Doenças Autoimunes/imunologia
Plexo Corióideo/imunologia
Infecção/imunologia
Células Mieloides/fisiologia
Doenças Neurodegenerativas/imunologia
Neuroimunomodulação
Ferimentos e Lesões/imunologia
[Mh] Termos MeSH secundário: Animais
Sistema Nervoso Central
Seres Humanos
Meninges/imunologia
Neuroproteção
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


  5 / 3264 MEDLINE  
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[PMID]:28636960
[Au] Autor:Chavan SS; Pavlov VA; Tracey KJ
[Ad] Endereço:Center for Biomedical Science, Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY 11030, USA; Center for Bioelectronic Medicine, Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY 11030, USA. Electronic address: schavan@northwell.edu.
[Ti] Título:Mechanisms and Therapeutic Relevance of Neuro-immune Communication.
[So] Source:Immunity;46(6):927-942, 2017 Jun 20.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Active research at the frontiers of immunology and neuroscience has identified multiple points of interaction and communication between the immune system and the nervous system. Immune cell activation stimulates neuronal circuits that regulate innate and adaptive immunity. Molecular mechanistic insights into the inflammatory reflex and other neuro-immune interactions have greatly advanced our understanding of immunity and identified new therapeutic possibilities in inflammatory and autoimmune diseases. Recent successful clinical trials using bioelectronic devices that modulate the inflammatory reflex to significantly ameliorate rheumatoid arthritis and inflammatory bowel disease provide a path for using electrons as a therapeutic modality for targeting molecular mechanisms of immunity. Here, we review mechanisms of peripheral sensory neuronal function in response to immune challenges, the neural regulation of immunity and inflammation, and the therapeutic implications of those mechanistic insights.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Sistema Imunitário
Doenças Inflamatórias Intestinais/imunologia
Neuroimunomodulação
Células Receptoras Sensoriais/fisiologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Seres Humanos
Imunidade Inata
Inflamação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


  6 / 3264 MEDLINE  
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[PMID]:28636959
[Au] Autor:Yoo BB; Mazmanian SK
[Ad] Endereço:Division of Biology & Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA. Electronic address: byoo@caltech.edu.
[Ti] Título:The Enteric Network: Interactions between the Immune and Nervous Systems of the Gut.
[So] Source:Immunity;46(6):910-926, 2017 Jun 20.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interactions between the nervous and immune systems enable the gut to respond to the variety of dietary products that it absorbs, the broad spectrum of pathogens that it encounters, and the diverse microbiome that it harbors. The enteric nervous system (ENS) senses and reacts to the dynamic ecosystem of the gastrointestinal (GI) tract by translating chemical cues from the environment into neuronal impulses that propagate throughout the gut and into other organs in the body, including the central nervous system (CNS). This review will describe the current understanding of the anatomy and physiology of the GI tract by focusing on the ENS and the mucosal immune system. We highlight emerging literature that the ENS is essential for important aspects of microbe-induced immune responses in the gut. Although most basic and applied research in neuroscience has focused on the brain, the proximity of the ENS to the immune system and its interface with the external environment suggest that novel paradigms for nervous system function await discovery.
[Mh] Termos MeSH primário: Sistema Nervoso Central/imunologia
Sistema Nervoso Entérico
Microbioma Gastrointestinal
Trato Gastrointestinal/fisiologia
Sistema Imunitário/imunologia
Imunidade nas Mucosas
Intestinos/imunologia
[Mh] Termos MeSH secundário: Animais
Exposição Ambiental
Trato Gastrointestinal/anatomia & histologia
Interações Hospedeiro-Patógeno
Seres Humanos
Neuroimunomodulação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


  7 / 3264 MEDLINE  
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[PMID]:28576938
[Au] Autor:Silva JR; Lopes AH; Talbot J; Cecilio NT; Rossato MF; Silva RL; Souza GR; Silva CR; Lucas G; Fonseca BA; Arruda E; Alves-Filho JC; Cunha FQ; Cunha TM
[Ad] Endereço:Department of Pharmacology.
[Ti] Título:Neuroimmune-Glia Interactions in the Sensory Ganglia Account for the Development of Acute Herpetic Neuralgia.
[So] Source:J Neurosci;37(27):6408-6422, 2017 Jul 05.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herpetic neuralgia is the most important symptom of herpes zoster disease, which is caused by Nevertheless, the pathophysiological mechanisms involved in herpetic neuralgia are not totally elucidated. Here, we examined the neuroimmune interactions at the sensory ganglia that account for the genesis of herpetic neuralgia using a murine model of Herpes Simplex Virus Type-1 (HSV-1) infection. The cutaneous HSV-1 infection of mice results in the development of a zosteriform-like skin lesion followed by a time-dependent increase in pain-like responses (mechanical allodynia). Leukocytes composed mainly of macrophages and neutrophils infiltrate infected DRGs and account for the development of herpetic neuralgia. Infiltrating leukocytes are responsible for driving the production of TNF, which in turn mediates the development of herpetic neuralgia through downregulation of the inwardly rectifying K channel Kir4.1 in satellite glial cells. These results revealed that neuroimmune-glia interactions at the sensory ganglia play a critical role in the genesis of herpetic neuralgia. In conclusion, the present study elucidates novel mechanisms involved in the genesis of acute herpetic pain and open new avenues for its control. Acute herpetic neuralgia is the most important symptom of herpes zoster disease and it is very difficult to treat. Using a model of peripheral infection of mice with HSV-1, we have characterized for the first time the neuroimmune-glia interactions in the sensory ganglia that account for the development of acute herpetic neuralgia. Among these mechanisms, leukocytes composed mainly of macrophages and neutrophils infiltrate infected sensory ganglia and are responsible for driving the production of TNF. TNF, via TNFR1, mediates herpetic neuralgia development through downregulation of the inwardly rectifying K channel Kir4.1 in satellite glial cells. This study elucidates novel mechanisms involved in the genesis of acute herpetic neuralgia and open new avenues for its control.
[Mh] Termos MeSH primário: Gânglios Sensitivos/imunologia
Leucócitos/imunologia
Neuralgia Pós-Herpética/imunologia
Neuroglia/imunologia
Neuroimunomodulação/imunologia
Células Receptoras Sensoriais/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Progressão da Doença
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2233-16.2017


  8 / 3264 MEDLINE  
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[PMID]:28566946
[Au] Autor:Deak T; Kudinova A; Lovelock DF; Gibb BE; Hennessy MB
[Ad] Endereço:Center for Affective Science and Department of Psychology, Binghamton University-State University of New York (SUNY), Binghamton, New York, USA.
[Ti] Título:A multispecies approach for understanding neuroimmune mechanisms of stress.
[So] Source:Dialogues Clin Neurosci;19(1):37-53, 2017 Mar.
[Is] ISSN:1958-5969
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The relationship between stress challenges and adverse health outcomes, particularly for the development of affective disorders, is now well established. The highly conserved neuroimmune mechanisms through which responses to stressors are transcribed into effects on males and females have recently garnered much attention from researchers and clinicians alike. The use of animal models, from mice to guinea pigs to primates, has greatly increased our understanding of these mechanisms on the molecular, cellular, and behavioral levels, and research in humans has identified particular brain regions and connections of interest, as well as associations between stress-induced inflammation and psychiatric disorders. This review brings together findings from multiple species in order to better understand how the mechanisms of the neuroimmune response to stress contribute to stress-related psychopathologies, such as major depressive disorder, schizophrenia, and bipolar disorder.
[Mh] Termos MeSH primário: Inflamação/imunologia
Transtornos Mentais/imunologia
Neuroimunomodulação/imunologia
Estresse Psicológico/imunologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Seres Humanos
Inflamação/fisiopatologia
Privação Materna
Transtornos Mentais/fisiopatologia
Fatores Sexuais
Isolamento Social
Estresse Fisiológico/imunologia
Estresse Psicológico/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE


  9 / 3264 MEDLINE  
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[PMID]:28566949
[Au] Autor:Tiwari PC; Pal R
[Ti] Título:The potential role of neuroinflammation and transcription factors in Parkinson disease.
[So] Source:Dialogues Clin Neurosci;19(1):71-80, 2017 Mar.
[Is] ISSN:1958-5969
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Parkinson disease (PD) is a neurodegenerative disorder characterized by dopaminergic neurons affected by inflammatory processes. Post-mortem analyses of brain and cerebrospinal fluid from PD patients show the accumulation of proinflammatory cytokines, confirming an ongoing neuroinflammation in the affected brain regions. These inflammatory mediators may activate transcription factors-notably nuclear factor κB, Ying-Yang 1 (YY1), fibroblast growth factor 20 (FGF20), and mammalian target of rapamycin (mTOR)-which then regulate downstream signaling pathways that in turn promote death of dopaminergic neurons through death domain-containing receptors. Dopaminergic neurons are vulnerable to oxidative stress and inflammatory attack. An increased level of inducible nitric oxide synthase observed in the substantia nigra and striatum of PD patients suggests that both cytokine-and chemokine-induced toxicity and inflammation lead to oxidative stress that contributes to degeneration of dopaminergic neurons and to disease progression. Lipopolysaccharide activation of microglia in the proximity of dopaminergic neurons in the substantia nigra causes their degeneration, and this appears to be a selective vulnerability of dopaminergic neurons to inflammation. In this review, we will look at the role of various transcription factors and signaling pathways in the development of PD.
[Mh] Termos MeSH primário: Inflamação/imunologia
Doença de Parkinson/imunologia
Fatores de Transcrição/imunologia
[Mh] Termos MeSH secundário: Seres Humanos
Inflamação/fisiopatologia
Neuroimunomodulação/imunologia
Doença de Parkinson/fisiopatologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE


  10 / 3264 MEDLINE  
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[PMID]:28566942
[Au] Autor:Thibaut F
[Ad] Endereço:University Hospital Cochin (Site Tarnier), Faculty of Medicine Paris Descartes, INSERM U 894, CNP, Paris, France.
[Ti] Título:Neuroinflammation: new vistas for neuropsychiatric research.
[So] Source:Dialogues Clin Neurosci;19(1):3-4, 2017 Mar.
[Is] ISSN:1958-5969
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:In psychiatric diseases such as mood disorders or schizophrenia, the inflammatory response system is activated. Microglia has gradually emerged as a key interface between stress-related signals and neuroimnune consequences of stress, with stressors leading to elevated microglial activity.
[Mh] Termos MeSH primário: Inflamação/imunologia
Transtornos Mentais/imunologia
Microglia/imunologia
Neuroimunomodulação/imunologia
[Mh] Termos MeSH secundário: Barreira Hematoencefálica/imunologia
Encéfalo/imunologia
Seres Humanos
Esquizofrenia/imunologia
Estresse Psicológico/imunologia
[Pt] Tipo de publicação:EDITORIAL; INTRODUCTORY JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE



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