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Journal of Neuroinflammation

John D Lee, Ning Liu, Samantha C Levin, Lars Ottosson, Ulf Andersson, Helena E Harris, Trent M Woodruff
BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressing neurodegenerative disease without effective treatment. The receptor for advanced glycation end products (RAGE) and the toll-like receptor (TLR) system are major components of the innate immune system, which have been implicated in ALS pathology. Extracellularly released high-mobility group box 1 (HMGB1) is a pleiotropic danger-associated molecular pattern (DAMP), and is an endogenous ligand for both RAGE and TLR4...
February 19, 2019: Journal of Neuroinflammation
Rodney M Ritzel, Abdullah Al Mamun, Joshua Crapser, Rajkumar Verma, Anita R Patel, Brittany E Knight, Nia Harris, Nickolas Mancini, Meaghan Roy-O'Reilly, Bhanu Priya Ganesh, Fudong Liu, Louise D McCullough
BACKGROUND: Ischemic stroke results in a robust inflammatory response within the central nervous system. As the immune-inhibitory CD200-CD200 receptor 1 (CD200R1) signaling axis is a known regulator of immune homeostasis, we hypothesized that it may play a role in post-stroke immune suppression after stroke. METHODS: In this study, we investigated the role of CD200R1-mediated signaling in stroke using CD200 receptor 1-deficient mice. Mice were subjected to a 60-min middle cerebral artery occlusion and evaluated at days 3 and 7, representing the respective peak and early resolution stages of neuroinflammation in this model of ischemic stroke...
February 18, 2019: Journal of Neuroinflammation
Liza Lind, Kristina Eriksson, Anna Grahn
BACKGROUND: Varicella-zoster virus (VZV) is a common viral agent causing central nervous system (CNS) infections including encephalitis, meningitis, and Ramsay Hunt syndrome. Neurological complications occur frequently despite antiviral treatment. Matrix metalloproteinases (MMPs) and cytokines are involved in the neuroinflammatory response during CNS infection. Their role in VZV CNS infections and how they differ between different CNS entities caused by VZV are poorly investigated. METHODS: We analyzed the levels of 30 chemokines and 9 MMPs in cerebrospinal fluid (CSF) and serum from 66 patients with VZV CNS infections diagnosed by detection of VZV DNA in CSF and concomitant neurological symptoms and compared with a control group (n = 24)...
February 18, 2019: Journal of Neuroinflammation
Kristin Mages, Felix Grassmann, Herbert Jägle, Rainer Rupprecht, Bernhard H F Weber, Stefanie M Hauck, Antje Grosche
BACKGROUND: Ligand-driven modulation of the mitochondrial translocator protein 18 kDa (TSPO) was recently described to dampen the neuroinflammatory response of microglia in a retinal light damage model resulting in protective effects on photoreceptors. We characterized the effects of the TSPO ligand XBD173 in the postischemic retina focusing on changes in the response pattern of the major glial cell types of the retina-microglia and Müller cells. METHODS: Retinal ischemia was induced by increasing the intraocular pressure for 60 min followed by reperfusion of the tissue in mice...
February 18, 2019: Journal of Neuroinflammation
Giuseppa Mudò, Monica Frinchi, Domenico Nuzzo, Pietro Scaduto, Fulvio Plescia, Maria F Massenti, Marta Di Carlo, Carla Cannizzaro, Giovanni Cassata, Luca Cicero, Maria Ruscica, Natale Belluardo, Luigi M Grimaldi
BACKGROUND: Aβ1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. METHODS: A rat model of AD was obtained by intra-hippocampal injection of Aβ1-42 peptide (23 μg/2 μl)...
February 18, 2019: Journal of Neuroinflammation
Young J Yauger, Sara Bermudez, Kasey E Moritz, Ethan Glaser, Bogdan Stoica, Kimberly R Byrnes
BACKGROUND: Excessive iron contributes to oxidative stress after central nervous system injury. NADPH oxidase (NOX) enzymes are upregulated in microglia after pro-inflammatory activation and contribute to oxidative stress. The relationship between iron, microglia, NOX, and oxidative stress is currently unclear. METHODS: We evaluated the effects of iron on lipopolysaccharide (LPS)-activated microglia and its secondary effect within neuronal co-cultures. Further, NOX2 and four specific inhibitors were tested to evaluate the relationship with the reactive oxygen species (ROS)-producing enzymes...
February 18, 2019: Journal of Neuroinflammation
Shoujiang You, Zhijie Ou, Wei Zhang, Danni Zheng, Chongke Zhong, Xiaofeng Dong, Chenhong Qiu, Taosheng Lu, Yongjun Cao, Chun-Feng Liu
BACKGROUND: High white blood cell (WBC) count and high blood glucose level are risk factors for mortality and pneumonia after acute ischemic stroke (AIS). We investigated the combined effect of high WBC count and high blood glucose level on hospital admission and in-hospital mortality and pneumonia in acute AIS patients. METHODS: A total of 3124 AIS patients enrolled from December 2013 to May 2014 across 22 hospitals in Suzhou city were included in the present study...
February 14, 2019: Journal of Neuroinflammation
Shoko Morita-Takemura, Kazuki Nakahara, Sanae Hasegawa-Ishii, Ayami Isonishi, Kouko Tatsumi, Hiroaki Okuda, Tatsuhide Tanaka, Masahiro Kitabatake, Toshihiro Ito, Akio Wanaka
BACKGROUND: Circulating endotoxins including lipopolysaccharides (LPS) cause brain responses such as fever and decrease of food and water intake, while pre-injection of endotoxins attenuates these responses. This phenomenon is called endotoxin tolerance, but the mechanisms underlying it remain unclear. The subfornical organ (SFO) rapidly produces proinflammatory cytokines including interleukin-1β (IL-1β) in response to peripherally injected LPS, and repeated LPS injection attenuates IL-1β production in the SFO, indicating that the SFO is involved in endotoxin tolerance...
February 14, 2019: Journal of Neuroinflammation
Christine Silwedel, Axel Haarmann, Markus Fehrholz, Heike Claus, Christian P Speer, Kirsten Glaser
BACKGROUND: Ureaplasma species (spp.) are commonly regarded as low-virulent commensals but may cause invasive diseases in immunocompromised adults and in neonates, including neonatal meningitis. The interactions of Ureaplasma spp. with host defense mechanisms are poorly understood. This study addressed Ureaplasma-driven cell death, concentrating on apoptosis as well as inflammatory cell death. METHODS: Human brain microvascular endothelial cells (HBMEC) were exposed to Ureaplasma (U...
February 14, 2019: Journal of Neuroinflammation
Wan-Chao Yang, Qi Wang, Lai-Ting Chi, Yue-Zhen Wang, Hong-Ling Cao, Wen-Zhi Li
BACKGROUND: This study investigated whether therapeutic hypercapnia (TH) ameliorated blood-brain barrier (BBB) damage and improved the neurologic outcome in a rat model of lateral fluid percussion injury (FPI), and explored the possible underlying mechanism. METHODS: Rats underwent lateral FPI and received inhalation of 30%O2 -70%N2 or 30%O2 -N2 plus CO2 to maintain arterial blood CO2 tension (PaCO2 ) between 80 and 100 mmHg for 3 h. To further explore the possible mechanisms for the protective effects of TH, a PKC inhibitor staurosporine or PKCαβ inhibitor GÖ6976 was administered via intracerebral ventricular injection...
February 13, 2019: Journal of Neuroinflammation
Shengchun Xu, Zemin Di, Yufeng He, Runjie Wang, Yuyang Ma, Rui Sun, Jing Li, Tao Wang, Yujun Shen, Shengyun Fang, Lijie Feng, Yuxian Shen
BACKGROUND: Extracellular accumulation of amyloid β-peptide (Aβ) is one of pathological hallmarks of Alzheimer's disease (AD) and contributes to the neuronal loss. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER) stress-inducible neurotrophic factor. Many groups, including ours, have proved that MANF rescues neuronal loss in several neurological disorders, such as Parkinson's disease and cerebral ischemia. However, whether MANF exerts its protective effect against Aβ neurotoxicity in AD remains unknown...
February 13, 2019: Journal of Neuroinflammation
Veronika E Neubrand, Irene Forte-Lago, Marta Caro, Mario Delgado
In the version of this article that was originally published [1]; some information in the "Author's contributions" section was omitted.
February 12, 2019: Journal of Neuroinflammation
Enshan Feng, Tingyu Liang, Xiaoyong Wang, Juan Du, Kai Tang, Xiaoxuan Wang, Fang Wang, Gan You
BACKGROUND: Human gliomas are highly fatal tumors with a significant feature of immune suppression. The association of the immune system in gliomas is gradually revealed, and immunotherapy is expected to improve the survival of glioma patients. In-depth understanding of the immune microenvironment of gliomas and their associated immunotherapy was increased exponentially in recent years. Gliomas provide clinical targets for immunotherapy during the search of key regulators of immune response...
February 12, 2019: Journal of Neuroinflammation
Hong-Chun Xiang, Li-Xue Lin, Xue-Fei Hu, He Zhu, Hong-Ping Li, Ru-Yue Zhang, Liang Hu, Wen-Tao Liu, Yi-Lin Zhao, Yang Shu, Hui-Lin Pan, Man Li
BACKGROUND: Chronic pain is a major clinical problem with limited treatment options. Previous studies have demonstrated that activation of adenosine monophosphate-activated protein kinase (AMPK) can attenuate neuropathic pain. Inflammation/immune response at the site of complete Freund's adjuvant (CFA) injection is known to be a critical trigger of the pathological changes that produce inflammatory pain. However, whether activation of AMPK produces an analgesic effect through inhibiting the proinflammatory cytokines, including interleukin-1β (IL-1β), in inflammatory pain remains unknown...
February 12, 2019: Journal of Neuroinflammation
Alexandre D Gimenes, Bruna F D Andrade, José Victor P Pinotti, Sonia M Oliani, Orfa Y Galvis-Alonso, Cristiane D Gil
BACKGROUND: The inflammatory process has been described as a crucial mechanism in the pathophysiology of temporal lobe epilepsy. The anti-inflammatory protein annexin A1 (ANXA1) represents an interesting target in the regulation of neuroinflammation through the inhibition of leukocyte transmigration and the release of proinflammatory mediators. In this study, the role of the ANXA1-derived peptide Ac2-26 in an experimental model of status epilepticus (SE) was evaluated. METHODS: Male Wistar rats were divided into Naive, Sham, SE and SE+Ac2-26 groups, and SE was induced by intrahippocampal injection of pilocarpine...
February 12, 2019: Journal of Neuroinflammation
Dylan J Finneran, Kevin R Nash
Alzheimer's disease (AD) is a progressive, neurodegenerative disorder, and the most common form of dementia. As the understanding of AD has progressed, it is now believed that AD is an amyloid-initiated tauopathy with neuroinflammation serving as the link between amyloid deposition, tau pathology, and neurodegeneration. As microglia are the main immune effectors in the central nervous system, they have been the focus of attention in studies investigating the neuroinflammatory component of AD. Therefore, recent work has focused on immunomodulators, which can alter microglial activation without suppressing activity, as potential therapeutics for AD...
February 11, 2019: Journal of Neuroinflammation
Huan-Huan Ding, Su-Bo Zhang, You-You Lv, Chao Ma, Meng Liu, Kui-Bo Zhang, Xiang-Cai Ruan, Jia-You Wei, Wen-Jun Xin, Shao-Ling Wu
BACKGROUND: Studies showed that upregulation of Nav1.6 increased the neuronal excitability and participated in neuropathic pain in the dorsal root ganglion (DRG). However, the molecular mechanisms underlying Nav1.6 upregulation were not reported yet. METHODS: The paw withdrawal threshold was measured in the rodents following lumbar 5 ventral root transection (L5-VRT). Then qPCR, western blotting, immunoprecipitation, immunohistochemistry, and chromatin immunoprecipitation assays were performed to explore the molecular mechanisms in vivo and in vitro...
February 8, 2019: Journal of Neuroinflammation
Brian Chiou, Elizabeth Neely, Asha Kallianpur, James R Connor
BACKGROUND: Inappropriate contact between the immune system and the central nervous system is thought to be a cause of demyelination. We previously reported the ability of the class IV semaphorin, Semaphorin4A (Sema4A), to induce apoptosis in human oligodendrocytes; however, these results have yet to be translated to an in vivo setting. Importantly, HIV-associated neurocognitive disorder remains a significant complication for patients on combined anti-retroviral therapy, with white matter damage seen on MRI...
February 8, 2019: Journal of Neuroinflammation
Stephanie W Lee, Juan Pablo de Rivero Vaccari, Jessie S Truettner, W Dalton Dietrich, Robert W Keane
BACKGROUND: Traumatic brain injury remains a significant cause of death and disability in the USA. Currently, there are no effective therapies to mitigate disability except for surgical interventions necessitating a need for continued research into uncovering novel therapeutic targets. In a recent study, we used a rodent model of penetrating traumatic brain injury known as penetrating ballistic-like brain injury (PBBI) to examine the role of innate immunity in post-traumatic secondary injury mechanisms...
February 8, 2019: Journal of Neuroinflammation
Carsten Balser, Anne Wolf, Marc Herb, Thomas Langmann
BACKGROUND: Age-related macular degeneration (AMD) is a leading cause of visual impairment in the elderly. The neovascular (wet) form of AMD can be treated with intravitreal injections of different anti-vascular endothelial growth factor (VEGF) agents. Placental growth factor (PGF) is another member of the VEGF family of cytokines with pro-angiogenic and pro-inflammatory effects. Here, we aimed to compare single and combined inhibition of VEGF-A and PGF in the laser-induced mouse model of choroidal neovascularization (CNV) with a focus on the effects on retinal mononuclear phagocytes...
February 7, 2019: Journal of Neuroinflammation
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