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TLR, brain

Raphaela Mayerhofer, Esther E Fröhlich, Florian Reichmann, Aitak Farzi, Nora Kogelnik, Eleonore Fröhlich, Wolfgang Sattler, Peter Holzer
Microbial metabolites are known to affect immune system, brain, and behavior via activation of pattern recognition receptors such as Toll-like receptor 4 (TLR4). Unlike the effect of the TLR4 agonist lipopolysaccharide (LPS), the role of other TLR agonists in immune-brain communication is insufficiently understood. We therefore hypothesized that the TLR2 agonist lipoteichoic acid (LTA) causes immune activation in the periphery and brain, stimulates the hypothalamic-pituitary-adrenal (HPA) axis and has an adverse effect on blood-brain barrier (BBB) and emotional behavior...
October 14, 2016: Brain, Behavior, and Immunity
Qi Zhong, Kai Zhou, Qiao-Li Liang, Sen Lin, Yan-Chun Wang, Xiao-Yi Xiong, Zhao-You Meng, Ting Zhao, Wen-Yao Zhu, Yuan-Rui Yang, Mao-Fan Liao, Qiu-Wen Gong, Liang Liu, Ao Xiong, Junwei Hao, Jian Wang, Qing-Wu Yang
BACKGROUND: Neuroinflammation plays a key role in intracerebral hemorrhage (ICH)-induced secondary brain injury, but the specific roles of peripheral inflammatory cells such as macrophages and lymphocytes remain unknown. The purpose of this study was to explore the roles of macrophages, T lymphocytes, and the cytokines they secrete as potential targets for treating secondary brain injury after ICH. METHODS AND RESULTS: Our results showed that peripheral macrophages and T lymphocytes successively infiltrated the brain, with macrophage counts peaking 1 day after ICH and T-lymphocyte counts peaking after 4 days...
October 11, 2016: Journal of the American Heart Association
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
Li-Xue Zhao, Jun-Rong Du, Hong-Jing Zhou, Dong-Ling Liu, Man-Xia Gu, Fang-Yi Long
BACKGROUND: Peroxiredoxins (Prxs) are proposed to function as damage-associated molecular patterns (DAMPs) and contribute to post-ischemic neuroinflammation and brain injury by activating Toll-like receptor (TLR) 4 at the acute and subacute phases after ischemic stroke. However, there are few studies concerning the inflammatory profiles of six distinct subtypes of Prxs (Prx1-Prx6). Our previous study demonstrated that the protective effect of ligustilide (LIG) against cerebral ischemia was associated with inhibition of neuroinflammatory response and Prx/TLR4 signaling in rats...
2016: PloS One
Chin-Yi Cheng, Yu-Chen Lee
Inflammation plays a crucial role in the pathophysiology of acute ischemic stroke. In the ischemic cascade, resident microglia are rapidly activated in the brain parenchyma and subsequently trigger inflammatory mediator release, which facilitates leukocyte-endothelial cell interactions in inflammation. Activated leukocytes invade the endothelial cell junctions and destroy the blood-brain barrier integrity, leading to brain edema. Toll-like receptors (TLRs) stimulation in microglia/macrophages through the activation of intercellular signaling pathways secretes various proinflammatory cytokines and enzymes and then aggravates cerebral ischemic injury...
2016: Evidence-based Complementary and Alternative Medicine: ECAM
Susan Cohen, Xingrao Ke, Qiuli Liu, Qi Fu, Amber Majnik, Robert Lane
BACKGROUND: Adverse maternal lifestyle resulting in adverse early life environment (AELE) increases risks for neuropsychiatric disorders in offspring. Neuropsychiatric disorders are associated with impaired neurogenesis and neuro-inflammation in the hippocampus (HP). Microglia are neuro-inflammatory cells in the brain that regulate neurogenesis via toll-like receptors (TLR). TLR-9 is implicated in neurogenesis inhibition and is responsible for stress-related inflammatory responses. We hypothesized that AELE would increase microglia cell count and increase TLR-9 expression in juvenile mouse HP...
September 22, 2016: International Journal of Developmental Neuroscience
Michelle Go, Jinghong Kou, Jeong-Eun Lim, Junling Yang, Ken-Ichiro Fukuchi
Microglia-mediated clearance of amyloid beta-protein (Aβ) via Toll-like receptor 4 (TLR4) signaling may play an important role in the pathogenesis of Alzheimer's disease (AD). However, as the disease progresses, activated microglia appear to become incapable of clearing Aβ deposits. Because repeated exposure to a TLR4 ligand leads to a diminished response of monocytes/macrophages to lipopolysaccharide (LPS) and because aggregated Aβ is a TLR4 ligand, we hypothesize that chronic exposure of microglia to Aβ deposits may induce a state of Toll-like receptor (TLR) signaling dysfunction, leading to decreased Aβ clearance and accelerated disease progression...
October 14, 2016: Biochemical and Biophysical Research Communications
Jing-Wen Yu, Yan-Hua Li, Guo-Bin Song, Jie-Zhong Yu, Chun-Yun Liu, Jian-Chun Liu, Hai-Fei Zhang, Wan-Fang Yang, Qing Wang, Ya-Ping Yan, Bao-Guo Xiao, Cun-Gen Ma
Bone marrow-derived mesenchymal stem cells (MSCs) are the ideal transplanted cells of cellular therapy for promoting neuroprotection and neurorestoration. However, the optimization of transplanted cells and the improvement of microenvironment around implanted cells are still two critical challenges for enhancing therapeutic effect. In the current study, we observed the therapeutic potential of MSCs combined with Fasudil in mouse model of experimental autoimmune encephalomyelitis (EAE) and explored possible mechanisms of action...
August 30, 2016: Journal of Molecular Neuroscience: MN
Masataka Ifuku, Alice Buonfiglioli, Philipp Jordan, Seija Lehnardt, Helmut Kettenmann
Microglial cells are the pathologic sensor of the brain, and any pathologic event triggers microglial activation, which involves migration of these cells to a lesion site. Employing different migration assays, we show that ligands for toll-like receptor (TLR) 2 stimulate random motility, while TLR7 ligands are chemoattractants. The subtype specificity of the TLR ligands was verified by using different TLR-deficient (TLRKO) mouse lines. PI3K and Rac inhibition impairs both TLR2- and TLR7-stimulated microglial migration...
November 2016: Brain, Behavior, and Immunity
Amin Mottahedin, Peter Lawrence Phillip Smith, Henrik Hagberg, C Joakim Ek, Carina Mallard
Inflammation is a significant risk factor for brain injury in the perinatal period. In this study, we tested the hypothesis that activation of peripheral TLR induces inflammation in the brain, including leukocyte trafficking. Postnatal day 8 mice were injected intraperitoneally with a TLR1/2 (Pam3CSK4, P3C), TLR2/6 (FSL-1) or TLR4 (LPS) agonist, and the peripheral and central cytokine and chemokine response was determined. Infiltration of immune cells to the CSF and brain was examined by flow cytometry, and brain permeability was investigated by radioactively labeled sucrose...
August 4, 2016: Journal of Leukocyte Biology
Claire L McDonald, Edel Hennessy, Ana Rubio Araiz, Brian Keogh, William McCormack, Peter McGuirk, Mary Reilly, Marina A Lynch
The effects of Toll-like receptor (TLR) activation in peripheral cells are well characterized but, although several TLRs are expressed on cells of the brain, the consequences of their activation on neuronal function remain to be fully investigated, particularly in the context of assessing their potential as therapeutic targets in neurodegenerative diseases. Several endogenous TLR ligands have been identified, many of which are soluble factors released from cells exposed to stressors. In addition, amyloid-β (Aβ) the main constituent of the amyloid plaques in Alzheimer's disease (AD), activates TLR2, although it has also been shown to bind to several other receptors...
July 12, 2016: Brain, Behavior, and Immunity
Yu Jiezhong, L I Yanhua, Liu Chunyun, Wang Qing, G U Qingfang, Wang Huiqing, Zhang Guangxian, Xiao Baoguo, M A Cungen
INTRODUCTION: Therapeutic strategies targeting Alzheimer's disease (AD)-related molecule β-amyloid (Aβ), Tau protein and BACE enzyme have been recently explored. However,the treatment effect for single target is not ideal. Based on multiaspect roles of Rho kinase (ROCK) inhibitor Fasudil on neuroprotection, neurorepair and immunomodulation, we observed therapeutic potential of Fasudil and explored possible mechanisms in APP/PS1 transgenic (Tg) mice, an animal model of AD. METHODS: APP/PS1 Tg mice were treated with Fasudil (25 mg/kg/day) for 2 months by intraperitoneal injection...
July 10, 2016: CNS & Neurological Disorders Drug Targets
Jenni E Anttila, Keith W Whitaker, Emily S Wires, Brandon K Harvey, Mikko Airavaara
Stroke is the leading cause of disability in adults. Drug treatments that target stroke-induced pathological mechanisms and promote recovery are desperately needed. In the brain, an ischemic event triggers major inflammatory responses that are mediated by the resident microglial cells. In this review, we focus on the microglia activation after ischemic brain injury as a target of immunomodulatory therapeutics. We divide the microglia-mediated events following ischemic stroke into three categories: acute, subacute, and long-term events...
July 4, 2016: Progress in Neuro-psychopharmacology & Biological Psychiatry
Yutaro Kobayashi, Hiroyuki Inagawa, Chie Kohchi, Katsuichiro Okazaki, Ran Zhang, Gen-Ichiro Soma
BACKGROUND/AIM: Monophosphoryl lipid A, lipopolysaccharide (LPS)-derived Toll-like receptor (TLR) 4 agonist, has been shown to be effective in the prevention of Alzheimer's disease (AD) by enhancing phagocytosis of amyloid β (Aβ) by brain microglia. Our recent study demonstrated that oral administration of LPS derived from Pantoea agglomerans (LPSp) activates peritoneal macrophages and enhances the phagocytic activity via TLR4 signaling pathway; however, the effect of LPSp on Aβ phagocytosis in microglia is still unknown...
July 2016: Anticancer Research
Bruce Teter, Mary Jo LaDu, Patrick M Sullivan, Sally A Frautschy, Greg M Cole
The Apolipoprotein E (ApoE) isotype ApoE4 is a prevalent genetic risk factor for Alzheimer's disease (AD) that can modulate systemic and central inflammation, independent of amyloid accumulation. Although disruption of innate immune toll receptor signaling is modulated by ApoE and observed in AD, ApoE isotype-specific effects remain poorly understood. Therefore, we examined the effect of the ApoE isotype on the brain levels of major regulators of TLR signaling including miR146a, a microRNA enriched in the brain...
August 3, 2016: Neuroreport
Samuel Burke Nanni, Jonathan Pratt, David Beauchemin, Khadidja Haidara, Borhane Annabi
The low-density lipoprotein receptor-related protein 1 (LRP-1) is a multiligand endocytic receptor, which plays a pivotal role in controlling cytoskeleton dynamics during cancer cell migration. Its rapid endocytosis further allows efficient clearance of extracellular ligands. Concanavalin-A (ConA) is a lectin used to trigger in vitro physiological cellular processes, including cytokines secretion, nitric oxide production, and T-lymphocytes activation. Given that ConA exerts part of its effects through cytoskeleton remodeling, we questioned whether it affected LRP-1 expression, intracellular trafficking, and cell surface function in grade IV U87 glioblastoma cells...
2016: Biomarkers in Cancer
Mahsa Sadeghi, Maghsoud Peeri, Mir-Jamal Hosseini
Early life stressful events have detrimental effects on the brain and behavior, which are associated with the development of depression. Immune-inflammatory responses have been reported to contribute in the pathophysiology of depression. Many studies have reported on the beneficial effects of exercise against stress. However, underlying mechanisms through which exercise exerts its effects were poorly studied. Therefore, it applied maternal separation (MS), as a valid animal model of early-life adversity, in rats from postnatal day (PND) 2 to 14 for 180min per day...
September 1, 2016: Physiology & Behavior
Yik Lung Chan, Sonia Saad, Carol Pollock, Brian Oliver, Ibrahim Al-Odat, Amgad A Zaky, Nicole Jones, Hui Chen
Maternal cigarette smoke exposure (SE) during gestation can cause lifelong adverse effects in the offspring's brain. Several factors may contribute including inflammation, oxidative stress and hypoxia, whose changes in the developing brain are unknown. Female Balb/c mice were exposed to cigarette smoke prior to mating, during gestation and lactation. Male offspring were studied at postnatal day (P) 1, P20 and 13 weeks (W13). SE dams had reduced inflammatory mediators (IL-1β, IL-6 and toll like receptor (TLR)4 mRNA), antioxidant (manganese superoxide dismutase (MnSOD)), and increased mitochondrial activities (OXPHOS-I, III and V) and protein damage marker nitrotyrosine...
2016: Scientific Reports
Alvaro G Alvarado, Justin D Lathia
Innate immunity has evolved as the front-line cellular defense mechanism to acutely sense and decisively respond to microenvironmental alterations. The Toll-like receptor (TLR) family activates signaling pathways in response to stimuli and is well-characterized in both resident and infiltrating immune cells during neural inflammation, injury, and degeneration. Innate immune signaling has also been observed in neural cells during development and disease, including in the stem and progenitor cells that build the brain and are responsible for its homeostasis...
July 2016: Trends in Neurosciences
Omar Dildar a Dzaye, Feng Hu, Katja Derkow, Verena Haage, Philipp Euskirchen, Christoph Harms, Seija Lehnardt, Michael Synowitz, Susanne A Wolf, Helmut Kettenmann
Peripheral macrophages and resident microglia constitute the dominant glioma-infiltrating cells. The tumor induces an immunosuppressive and tumor-supportive phenotype in these glioma-associated microglia/brain macrophages (GAMs). A subpopulation of glioma cells acts as glioma stem cells (GSCs). We explored the interaction between GSCs and GAMs. Using CD133 as a marker of stemness, we enriched for or deprived the mouse glioma cell line GL261 of GSCs by fluorescence-activated cell sorting (FACS). Over the same period of time, 100 CD133(+ )GSCs had the capacity to form a tumor of comparable size to the ones formed by 10,000 CD133(-) GL261 cells...
May 2016: Journal of Neuropathology and Experimental Neurology
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