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Journal of Neuroimmunology

Pietro Maggi, Pascal Sati, Luca Massacesi
Magnetic resonance imaging (MRI) is an invaluable tool for the diagnosis and monitoring of patients with multiple sclerosis (MS) as well as for the study of the disease pathophysiology. Because of its strong clinical, radiological and histopathological similarities with the human disease, experimental autoimmune encephalomyelitis (EAE) in the common marmoset has been studied more intensively over the past several years. Here, we review the current knowledge on MRI in the marmoset EAE, and we outline the physiopathological significance and translational values of these studies with respect to MS...
October 8, 2016: Journal of Neuroimmunology
Daniel S Reich
Magnetic resonance imaging (MRI) has led to the identification of widespread brain abnormalities in multiple sclerosis (MS) that extend far beyond the classic white matter lesion. These findings have generated the idea that MS should be understood as a disease of the whole brain, not just the white matter. While it is no doubt the case that many different pathways are ultimately involved in the destruction of brain tissue that occurs in MS, the implications of the accumulated evidence for understanding disease pathophysiology - and hence the overall significance of these imaging findings - are doubtful...
October 3, 2016: Journal of Neuroimmunology
Amy E Lovett-Racke
This article is a summary of a lecture presented at the 40years of Neuroimmunology meeting held on April 19, 2015, in commemoration of the 40th anniversary of the Neuroimmunology Branch (NIB) at the National Institutes of Health. Experimental autoimmune encephalomyelitis (EAE) has been used as a model for multiple sclerosis (MS) for several decades. There are remarkable similarities between the central nervous system pathology of mice with EAE and MS patients. However, there are distinct differences which limits the contribution of EAE to the understanding of MS...
August 12, 2016: Journal of Neuroimmunology
Yoshihisa Yamano, Ariella Coler-Reilly
The main feature of Human T-lymphotropic virus type I (HTLV-1) -associated myelopathy/tropical spastic paraparesis (HAM/TSP) pathogenesis is a virus-induced hyperactive immune response that produces chronic inflammation in the central nervous system (CNS), but the mechanism by which HTLV-1 deregulates the immune response is unknown. We recently reported a high frequency of HTLV-1-infected CCR4(+) cells, including regulatory T cells. We showed that HTLV-1 induces a Th1-like state in these CCR4(+) cells via T-bet expression...
August 12, 2016: Journal of Neuroimmunology
Darrell Sawmiller, Ahsan Habib, Song Li, Donna Darlington, Huayan Hou, Jun Tian, R Douglas Shytle, Adam Smith, Brian Giunta, Takashi Mori, Jun Tan
Naturally-occurring bioactive flavonoids such as diosmin significantly reduces amyloid beta (Aβ) associated pathology in Alzheimer's disease (AD) mouse models. In the present study, oral administration of diosmin reduced cerebral Aβ oligomer levels, tau-hyperphosphorylation and cognitive impairment in the 3xTg-AD mouse model through glycogen synthase kinase-3 (GSK-3) and transient receptor potential canonical 6-related mechanisms. Diosmetin, one major bioactive metabolite of diosmin, increased inhibitory GSK-3β phosphorylation, while selectively reducing γ-secretase activity, Aβ generation, tau hyperphosphorylation and pro-inflammatory activation of microglia in vitro, without altering Notch processing...
October 15, 2016: Journal of Neuroimmunology
Martin Böhland, Eugenia Kress, Matthias B Stope, Thomas Pufe, Simone C Tauber, Lars-Ove Brandenburg
Bacterial meningitis is - despite therapeutical progress during the last decades - still characterized by high mortality and severe permanent neurogical sequelae. The brain is protected from penetrating pathogens by both the blood-brain barrier and the innate immune system. Invading pathogens are recognized by so-called pattern recognition receptors including the Toll-like receptors (TLR) which are expressed by glial immune cells in the central nervous system. Among these, TLR2 is responsible for the detection of Gram-positive bacteria such as the meningitis-causing pathogen Streptococcus pneumoniae...
October 15, 2016: Journal of Neuroimmunology
Jeroen Melief, Jan W Koper, Erik Endert, Holger J Møller, Jörg Hamann, Bernard M Uitdehaag, Inge Huitinga
As high cortisol levels are implicated in suppressed disease activity of multiple sclerosis (MS), glucocorticoid receptor (GR) polymorphisms that affect glucocorticoid (GC) sensitivity may impact on this by changing local immunomodulation or regulation of the hypothalamus-pituitary-adrenal (HPA)-axis. In this post-mortem study, we investigated whether GR haplotypes affect MS disease course and production of cortisol and soluble CD163 (sCD163), a molecule induced by GC on microglia/macrophages. We found that GR haplotypes that confer high GC sensitivity are associated with more aggressive MS but do not affect levels of cortisol secreted by the HPA-axis or shedding of CD163...
October 15, 2016: Journal of Neuroimmunology
Chiara Fenoglio, Milena De Riz, Anna M Pietroboni, Alberto Calvi, Maria Serpente, Sara M G Cioffi, Marina Arcaro, Emanuela Oldoni, Elio Scarpini, Daniela Galimberti
MicroRNAs (miRNAs) have recently found to be dysregulated in serum from multiple sclerosis (MS) patients. Cell free circulating miR-15b, -23a and 223 levels were analyzed by Real Time PCR in a cohort consisting of 30 serum samples from Relapsing Remitting MS patients at baseline (T0) and after three, six, nine and twelve months (T1, T2, T3, T4) after starting the treatment. A down-regulation of miRNA levels in patients at T0 compared with controls was present (p<0.001). MiRNA levels slightly increased at T1 and this trend reached the statistical significance at T2 vs T0 and remains stable at T3 and T4...
October 15, 2016: Journal of Neuroimmunology
Denise S M Medrado da Costa, Joana Hygino, Thais B Ferreira, Taissa M Kasahara, Priscila O Barros, Clarice Monteiro, Aleida Oliveira, Felipe Tavares, Claudia Cristina Vasconcelos, Regina Alvarenga, Cleonice A M Bento
Vitamin D deficiency is an environmental risk factor for MS, a Th17 cell-mediated autoimmune disease that results in demyelination in the CNS. Therefore, we aimed to evaluate the ability of in vitro 1,25(OH)2D in modulating different Th17 cell subsets in MS patients in remission phase. In the present study, the production of Th17-related cytokines (IL-1β, IL-6, IL-17, IL-22), as well as GM-CSF, was significantly higher in cell cultures from MS patients than in healthy subjects (HS). The 1,25(OH)2D reduced all pro-inflammatory cytokines essayed, mainly those released from HS cell cultures...
October 15, 2016: Journal of Neuroimmunology
Ling Li, Tingjun Dai, Chuanzhu Yan
No abstract text is available yet for this article.
October 15, 2016: Journal of Neuroimmunology
Mario A Pulido, Meleeneh Kazarian DerHartunian, Zhenxia Qin, Eric M Chung, Diane S Kang, Andrew W Woodham, Jeffrey A Tsou, Rinse Klooster, Omid Akbari, Lina Wang, W Martin Kast, Stephen V Liu, Jan J G M Verschuuren, Dana W Aswad, Ite A Laird-Offringa
Autoantibodies against SCLC-associated neuronal antigen ELAVL4 (HuD) have been linked to smaller tumors and improved survival, but the antigenic epitope and mechanism of autoimmunity have never been solved. We report that recombinant human ELAVL4 protein incubated under physiological conditions acquires isoaspartylation, a type of immunogenic protein damage. Specifically, the N-terminal region of ELAVL4, previously implicated in SCLC-associated autoimmunity, undergoes isoaspartylation in vitro, is recognized by sera from anti-ELAVL4 positive SCLC patients and is highly immunogenic in subcutaneously injected mice and in vitro stimulated human lymphocytes...
October 15, 2016: Journal of Neuroimmunology
Xiaonan Zhong, Honghao Wang, Zhiwei Ye, Wei Qiu, Zhengqi Lu, Rui Li, Yaqing Shu, Yanyu Chang, Xueqiang Hu
It is believed that auto-inflammatory activity, including cellular and humoral immunity responses, especially T cell-B cell collaboration, is one of the most important components of the pathogenesis of inflammatory demyelinating disease. CD40L is critical for T cell-B cell collaboration. Actually, serum CD40L levels have been shown to increase in MS. In the present study, serum CD40L levels were measured by an enzyme-linked immunosorbent assay (ELISA) in NMO (n=27) and MS (n=19) patients and controls (n=14)...
October 15, 2016: Journal of Neuroimmunology
Vadim Gospodarev, Justin Câmara, Vikram Chakravarthy, Arie Perry, Matthew Wood, Robin Dietz, Jun Wang, Kenneth De Los Reyes, Ravi Raghavan
IgG4-related pachymeningitis is a serious inflammatory condition that can present with symptoms of mass effect and focal deficits. The first-line therapy is steroids and second-line is chemotherapy (methotrexate, azathioprine, etc.). We describe a patient with IgG4-related pachymeningitis in whom steroid use was contraindicated and methotrexate was ineffective. During the course of treatment, the patient presented to the emergency department with receptive and expressive aphasia, slurred speech, right-sided neglect, and loss of sensation...
October 15, 2016: Journal of Neuroimmunology
Mariela Bettini, Hernan Gonorazky, Marcelo Chaves, Ernesto Fulgenzi, Alejandra Figueredo, Silvia Christiansen, Edgardo Cristiano, Enrico S Bertini, Marcelo Rugiero
Cases of acquired rippling muscle disease in association with myasthenia gravis have been reported. We present three patients with iRMD (immune-mediated rippling muscle disease) and AChR-antibody positive myasthenia gravis. None of them had thymus pathology. They presented exercise-induced muscle rippling combined with generalized myasthenia gravis. One of them had muscle biopsy showing a myopathic pattern and a patchy immunostaining with caveolin antibodies. They were successfully treated steroids and azathioprine...
October 15, 2016: Journal of Neuroimmunology
Sven Briken, Sina Cathérine Rosenkranz, Oliver Keminer, Stefan Patra, Gesche Ketels, Christoph Heesen, Rainer Hellweg, Ole Pless, Karl-Heinz Schulz, Stefan M Gold
BACKGROUND: Clinical studies have suggested beneficial effects of exercise on cognitive function in ageing adults and neurodegenerative diseases such as dementia. Recent work indicates the same for progressive multiple sclerosis (MS), an inflammatory and degenerative disease of the central nervous system (CNS). The biological pathways associated with these effects are however not well understood. OBJECTIVE: In this randomized controlled study, we explored serum levels of the myokine Irisin, the neurotrophin brain-derived neurotrophic factor (BDNF) and Interleukin-6 (IL-6) during acute endurance exercise and over the course of a 9-weeks endurance exercise training period in n=42 patients with progressive MS...
October 15, 2016: Journal of Neuroimmunology
Jueqiong Wang, Congying Zhao, Peng Kong, Guanyun Bian, Zhe Sun, Yafei Sun, Li Guo, Bin Li
Methylene blue (MB) is an effective neuroprotectant in many neurological disorders. AMP-activated protein kinase (AMPK)/silent mating-type information regulation 2 homolog 1 (SIRT1) plays a crucial role in maintaining inflammatory responses and shows a synergistic effect on cell homeostasis. We investigated the effect of MB on experimental autoimmune encephalomyelitis (EAE), a classical animal model of multiple sclerosis (MS). MB treatment reduced the clinical scores of EAE significantly and attenuated pathological injuries in spinal cords...
October 15, 2016: Journal of Neuroimmunology
Haiyan Peng, Huo Li, Adam Sheehy, Patrick Cullen, Norm Allaire, Robert H Scannevin
Delayed-release dimethyl fumarate (DMF) is an approved treatment for multiple sclerosis (MS). Microglia are considered central to MS pathophysiology, however the effects of DMF and the primary metabolite monomethyl fumarate (MMF) on microglia are not well characterized. We demonstrated that DMF and MMF altered transcriptional responses in primary microglia related to the nuclear factor (erythroid-derived 2)-like 2 pathway. Additionally, through an NRF2 independent manner, DMF, but not MMF significantly reduced production of proinflammatory mediators in classically activated microglia, and further rescued mitochondrial respiratory deficits in primary cortical neurons that were induced by activated microglia...
October 15, 2016: Journal of Neuroimmunology
Hui Shi, Kuang Zheng, Zulu Su, Hai Su, Ming Zhong, Xuenong He, Changlong Zhou, Hao Chen, Qijiang Xiong, Yi Zhang
Microglia polarization plays a vital role in brain inflammatory injury following intracerebral hemorrhage (ICH). Previous studies have shown that sinomenine possesses potential immunoregulatory capabilities. However, microglia polarization's exact mechanisms in ICH remain uncertain. Therefore, we examined the role of sinomenine on microglia polarization and brain inflammation following ICH. For the experiment, autologous blood models were constructed in C57/BL6 mice. Markers of classically activated (M1) and alternatively activated (M2) microglia were detected by real-time polymerase chain reaction, immunofluorescence, and flow cytometry...
October 15, 2016: Journal of Neuroimmunology
Alexander W M Hooper, Suleiman A Igdoura
Microgliosis and astrogliosis are known to be exacerbating factors in the progression of the lysosomal storage disorder Sandhoff disease. We have also found evidence for excitotoxicity via glutamate receptors in Sandhoff disease. To view the interaction of these cascades, we measured cerebellar expression of markers for gliosis, apoptosis, and excitatory synapses over the disease course in a Sandhoff disease mouse model. We observe a 2-stage model, with initial activation of microgliosis as early as 60days of age, followed by a later onset of astrogliosis, caspase-mediated apoptosis, and reduction in GluR1 at approximately 100days of age...
October 15, 2016: Journal of Neuroimmunology
Li Chen, Yanjun Zhang, Daojing Li, Nong Zhang, Ruiqiong Liu, Bin Han, Changjuan Wei, Haijie Liu, Xiaolin Xu, Junwei Hao
Vascular dementia (VaD) is a widely prevalent and devastating disease. Despite the tremendous complexity that limits understanding of the pathophysiology of VaD, microglial dysfunction has been attributed, in part, to immune microenviroment disorder and finally leads to cognitive deficits. Considered the mammalian target of rapamycin complex 1 (mTORC1) is a key player in regulation of glial function, our work focused on whether the mTOR inhibitor everolimus (RAD001) could overcome the destructive microglial function, change the phenotype and ameliorate cognitive decline induced by chronic cerebral hypoperfusion...
October 15, 2016: Journal of Neuroimmunology
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