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Myelin Cx3cr1

Harald Lund, Melanie Pieber, Roham Parsa, David Grommisch, Ewoud Ewing, Lara Kular, Jinming Han, Keying Zhu, Jik Nijssen, Eva Hedlund, Maria Needhamsen, Sabrina Ruhrmann, André Ortlieb Guerreiro-Cacais, Rasmus Berglund, Maria J Forteza, Daniel F J Ketelhuth, Oleg Butovsky, Maja Jagodic, Xing-Mei Zhang, Robert A Harris
The cytokine transforming growth factor-β (TGF-β) regulates the development and homeostasis of several tissue-resident macrophage populations, including microglia. TGF-β is not critical for microglia survival but is required for the maintenance of the microglia-specific homeostatic gene signature1,2 . Under defined host conditions, circulating monocytes can compete for the microglial niche and give rise to long-lived monocyte-derived macrophages residing in the central nervous system (CNS)3-5 . Whether monocytes require TGF-β for colonization of the microglial niche and maintenance of CNS integrity is unknown...
April 16, 2018: Nature Immunology
Zorica Stojić-Vukanić, Ivan Pilipović, Jasmina Djikić, Ivana Vujnović, Mirjana Nacka-Aleksić, Biljana Bufan, Nevena Arsenović-Ranin, Duško Kosec, Gordana Leposavić
The study investigated strain specificities in age-related differences in CD8+ T cell- and microglial cell-mediated mechanisms implicated in induction/perpetuation and/or control of neuroinflammation in experimental autoimmune encephalomyelitis (EAE) in Albino Oxford (AO) and Dark Agouti (DA) rats exhibiting age-related changes in the susceptibility to EAE in the opposite direction (increase in relatively resistant AO rats vs decrease in DA rats). In the inductive phase of EAE, the greater number of fully differentiated effector CD8+ T lymphocytes was found in draining lymph nodes (dLNs) from aged rats of both strains than in strain-matched young rats, but this was particularly prominent in AO rats, which exhibited milder EAE of prolonged duration compared with their DA counterparts...
January 2018: Experimental Gerontology
Sinead A O'Sullivan, Kumlesh K Dev
BACKGROUND: Fractalkine/CX3CR1 signalling has been implicated in many neurodegenerative and neurological diseases of the central nervous system (CNS). This signalling pathway plays an important role in regulating reactive oxygen species (ROS), as well as itself being altered in conditions of oxidative stress. Here, we investigated the effects of recombinant fractalkine (rCX3CL1) in models of hydrogen peroxide (H2O2)-induced demyelination and astrocyte toxicity, within organotypic cerebellar slice cultures...
August 15, 2017: Journal of Neuroinflammation
Tzu-Ying Chuang, Yong Guo, Scott M Seki, Abagail M Rosen, David M Johanson, James W Mandell, Claudia F Lucchinetti, Alban Gaultier
Multiple sclerosis is a devastating neurological disorder characterized by the autoimmune destruction of the central nervous system myelin. While T cells are known orchestrators of the immune response leading to MS pathology, the precise contribution of CNS resident and peripheral infiltrating myeloid cells is less well described. Here, we explore the myeloid cell function of Low-density lipoprotein receptor-related protein-1 (LRP1), a scavenger receptor involved in myelin clearance and the inflammatory response, in the context of Multiple sclerosis...
July 11, 2016: Acta Neuropathologica Communications
Xiao-Mei Wu, Yong Liu, Zhong-Ming Qian, Qian-Qian Luo, Ya Ke
Based on current knowledge on the role of the CX3CL1/CX3CR1 axis in the regulation of microglial activation and on the involvement of activated microglia in damaging oligodendrocytes, we hypothesized that CX3CL1/CX3CR1 axis is associated with the development of ischemic oligodendrocyte and white matter injury. We investigated the effects of CX3CL1, CX3CR1 shRNA, and p38MAPK inhibitor on the apoptosis, proliferation, and myelin proteolipid protein (PLP) expression in oligodendrocytes in co-cultures with BV2 microglia under ischemia...
August 2016: Molecular Neurobiology
Filipa L Cardoso, Jasmin Herz, Adelaide Fernandes, João Rocha, Bruno Sepodes, Maria A Brito, Dorian B McGavern, Dora Brites
BACKGROUND: The inflammatory mediator lipopolysaccharide (LPS) has been shown to induce acute gliosis in neonatal mice. However, the progressive effects on the murine neurodevelopmental program over the week that follows systemic inflammation are not known. Thus, we investigated the effects of repeated LPS administration in the first postnatal week in mice, a condition mimicking sepsis in late preterm infants, on the developing central nervous system (CNS). METHODS: Systemic inflammation was induced by daily intraperitoneal administration (i...
2015: Journal of Neuroinflammation
Antoine Lampron, Antoine Larochelle, Nathalie Laflamme, Paul Préfontaine, Marie-Michèle Plante, Maria Gabriela Sánchez, V Wee Yong, Peter K Stys, Marie-Ève Tremblay, Serge Rivest
An imbalance between remyelinating and demyelinating rates underlies degenerative processes in demyelinating diseases such as multiple sclerosis. An optimal therapeutic strategy would be to stimulate remyelination while limiting demyelination. Although accumulation of myelin debris impairs remyelination, the mechanisms regulating the clearance of such debris by mononuclear phagocytic cells are poorly understood. We demonstrate that after cuprizone intoxication, CCR2-dependent infiltration of mouse bone marrow-derived cells is abundant in demyelinating areas, but that these cells do not impact demyelination...
April 6, 2015: Journal of Experimental Medicine
Xi Wang, Kai Cao, Xin Sun, Yongxiong Chen, Zhaoxia Duan, Li Sun, Lei Guo, Paul Bai, Dongming Sun, Jianqing Fan, Xijing He, Wise Young, Yi Ren
Macrophage activation and persistent inflammation contribute to the pathological process of spinal cord injury (SCI). It was reported that M2 macrophages were induced at 3-7 days after SCI but M2 markers were reduced or eliminated after 1 week. By contrast, M1 macrophage response is rapidly induced and then maintained at injured spinal cord. However, factors that modulate macrophage phenotype and function are poorly understood. We developed a model to distinguish bone-marrow derived macrophages (BMDMs) from residential microglia and explored how BMDMs change their phenotype and functions in response to the lesion-related factors in injured spinal cord...
April 2015: Glia
Anne C Solga, Winnie W Pong, Jason Walker, Todd Wylie, Vincent Magrini, Anthony J Apicelli, Malachi Griffith, Obi L Griffith, Shinichi Kohsaka, Gregory F Wu, David L Brody, Elaine R Mardis, David H Gutmann
Expression profiling of distinct central nervous system (CNS) cell populations has been employed to facilitate disease classification and to provide insights into the molecular basis of brain pathology. One important cell type implicated in a wide variety of CNS disease states is the resident brain macrophage (microglia). In these studies, microglia are often isolated from dissociated brain tissue by flow sorting procedures [fluorescence-activated cell sorting (FACS)] or from postnatal glial cultures by mechanic isolation...
April 2015: Glia
Anna Ridderstad Wollberg, Anders Ericsson-Dahlstrand, Anders Juréus, Petra Ekerot, Sylvia Simon, Maria Nilsson, Stig-Johan Wiklund, Anna-Lena Berg, Mats Ferm, Dan Sunnemark, Rolf Johansson
One hallmark of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is infiltration of leukocytes into the CNS, where chemokines and their receptors play a major mediatory role. CX3CR1 is a chemokine receptor involved in leukocyte adhesion and migration and hence a mediator of immune defense reactions. The role of CX3CR1 in MS and EAE pathogenesis however remains to be fully assessed. Here, we demonstrate CX3CR1 mRNA expression on inflammatory cells within active plaque areas in MS brain autopsies...
April 8, 2014: Proceedings of the National Academy of Sciences of the United States of America
Rebecca A Sosa, Cathi Murphey, Niannian Ji, Astrid E Cardona, Thomas G Forsthuber
Induction of experimental autoimmune encephalomyelitis (EAE) in susceptible animals requires reactivation of encephalitogenic CD4(+) T cells by APCs in the CNS. However, it has remained unresolved from where APCs in the CNS acquire myelin Ag for T cell activation and under which conditions, that is, whether only during EAE or also in the naive CNS. In this study, we investigated the kinetics of myelin Ag uptake by CNS APCs during EAE and in the naive CNS. Our results show that during EAE CX3CR1(+)CD11b(+) microglia were the first APCs in the CNS to contain myelin Ag upon induction of disease, albeit in very small numbers...
December 15, 2013: Journal of Immunology: Official Journal of the American Association of Immunologists
Wenjun Zhu, Crystal Acosta, Brian MacNeil, Claudia Cortes, Howard Intrater, Yuewen Gong, Mike Namaka
Multiple sclerosis (MS) is a central nervous system (CNS) disease resulting from a targeted autoimmune-mediated attack on myelin proteins in the CNS. The release of Th1 inflammatory mediators in the CNS activates macrophages, antibodies, and microglia resulting in myelin damage and the induction of neuropathic pain (NPP). Molecular signaling through fractalkine (CX3CL1), a nociceptive chemokine, via its receptor (CX3CR1) is thought to be associated with MS-induced NPP. An experimental autoimmune encephalomyelitis (EAE) model of MS was utilized to assess time dependent gene and protein expression changes of CX3CL1 and CX3CR1...
2013: BioMed Research International
Jenny A Garcia, Paula A Pino, Makiko Mizutani, Sandra M Cardona, Israel F Charo, Richard M Ransohoff, Thomas G Forsthuber, Astrid E Cardona
Fractalkine, a chemokine anchored to neurons or peripheral endothelial cells, serves as an adhesion molecule or as a soluble chemoattractant. Fractalkine binds CX3CR1 on microglia and circulating monocytes, dendritic cells, and NK cells. The aim of this study is to determine the role of CX3CR1 in the trafficking and function of myeloid cells to the CNS during experimental autoimmune encephalomyelitis (EAE). Our results show that, in models of active EAE, Cx3cr1(-/-) mice exhibited more severe neurologic deficiencies...
August 1, 2013: Journal of Immunology: Official Journal of the American Association of Immunologists
Dustin J Donnelly, Erin E Longbrake, Todd M Shawler, Kristina A Kigerl, Wenmin Lai, C Amy Tovar, Richard M Ransohoff, Phillip G Popovich
Macrophages exert divergent effects in the injured CNS, causing either neurotoxicity or regeneration. The mechanisms regulating these divergent functions are not understood but can be attributed to the recruitment of distinct macrophage subsets and the activation of specific intracellular signaling pathways. Here, we show that impaired signaling via the chemokine receptor CX3CR1 promotes recovery after traumatic spinal cord injury (SCI) in mice. Deficient CX3CR1 signaling in intraspinal microglia and monocyte-derived macrophages (MDMs) attenuates their ability to synthesize and release inflammatory cytokines and oxidative metabolites...
July 6, 2011: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Diego Gomez-Nicola, Alessandra Spagnolo, Carmen Guaza, Manuel Nieto-Sampedro
IL-15 initially identified as a T proliferating cytokine has several structural and biological similarities with IL-2 and has been associated with a number of autoimmune diseases. Because of the scarcity of information available on the role of IL-15 in MS pathogenesis, we have investigated how the absence of IL-15 affected the development of experimental autoimmune encephalomyelitis, a mouse model of MS. Following immunization of IL-15(-/-) and C57BL/6 mice with MOG(35-55), we observed a more severe neurological impairment in the IL-15 knockout mice than in the wild-type group...
April 2010: Experimental Neurology
Dan Sunnemark, Sana Eltayeb, Maria Nilsson, Erik Wallström, Hans Lassmann, Tomas Olsson, Anna-Lena Berg, Anders Ericsson-Dahlstrand
BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It is associated with local activation of microglia and astroglia, infiltration of activated macrophages and T cells, active degradation of myelin and damage to axons and neurons. The proposed role for CX3CL1 (fractalkine) in the control of microglia activation and leukocyte infiltration places this chemokine and its receptor CX3CR1 in a potentially strategic position to control key aspects in the pathological events that are associated with development of brain lesions in MS...
July 29, 2005: Journal of Neuroinflammation
Dan Sunnemark, Sana Eltayeb, Erik Wallström, Lena Appelsved, Asa Malmberg, Hans Lassmann, Anders Ericsson-Dahlstrand, Fredrik Piehl, Tomas Olsson
Chemokines are important for the recruitment of immune cells into sites of inflammation. To better understand their functional roles during inflammation we have here studied the in vivo expression of receptors for the chemokines CCL3/CCL5/CCL7 (MIP-1alpha/RANTES/MCP-3) and CX3CL1 (fractalkine), CCR1 and CX3CR1, respectively, in rat myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis. Combined in situ hybridization and immunohistochemistry demonstrated intensely upregulated CCR1 mRNA expression in early, actively demyelinating plaques, whereas CX3CR1 displayed a more generalized expression pattern...
October 2003: Brain Pathology
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