The Experts below are selected from a list of 663 Experts worldwide ranked by ideXlab platform
Subramaniam Sriram - One of the best experts on this subject based on the ideXlab platform.
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Anacardic acid induces IL-33 and promotes remyelination in CNS.
Proceedings of the National Academy of Sciences of the United States of America, 2020Co-Authors: Asa Ljunggren-rose, Chandramohan Natarajan, Pranathi Matta, Akansha Pandey, Isha Upender, Subramaniam SriramAbstract:Given the known neuroreparative actions of IL-33 in Experimental models of central nervous system (CNS) injury, we predicted that compounds which induce IL-33 are likely to promote remyelination. We found anacardic acid as a candidate molecule to serve as a therapeutic agent to promote remyelination. Addition of anacardic acid to cultured oligodendrocyte precursor cells (OPCs) rapidly increased expression of myelin genes and myelin proteins, suggesting a direct induction of genes involved in myelination by anacardic acid. Also, when added to OPCs, anacardic acid resulted in the induction of IL-33. In vivo, treatment of with anacardic acid in doses which ranged from 0.025 mg/kg to 2.5 mg/kg, improved pathologic scores in Experimental Allergic Encephalitis (EAE) and in the cuprizone model of demyelination/remyelination. Electron microscopic studies performed in mice fed with cuprizone and treated with anacardic acid showed lower g-ratio scores when compared to controls, suggesting increased remyelination of axons. In EAE, improvement in paralytic scores was seen when the drug was given prior to or following the onset of paralytic signs. In EAE and in the cuprizone model, areas of myelin loss, which are likely to remyelinate, was associated with a greater recruitment of IL-33-expressing OPCs in mice which received anacardic acid when compared to controls.
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Brief Definitive Report Chlamydia pneumoniae Infection of the Central Nervous System Worsens Experimental Allergic Encephalitis
2013Co-Authors: Song-yi Yao, Asa Ljunggren-rose, Subramaniam SriramAbstract:Experimental Allergic Encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae, after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease. Key words: Chlamydia • autoimmunity • multiple sclerosis • demyelination • bystander activatio
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Chlamydia pneumoniae Infection of the Central Nervous System Worsens Experimental Allergic Encephalitis
The Journal of experimental medicine, 2002Co-Authors: Song-yi Yao, Asa Ljunggren-rose, Subramaniam SriramAbstract:Experimental Allergic Encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae , after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae , and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease.
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Immunotherapy of inflammatory demyelinating diseases of the central nervous system
Immunologic Research, 2001Co-Authors: Johu J. Bright, Subramaniam SriramAbstract:Inflammatory demyelinating diseases comprise a heterogeneous group of disorders that affect the peripheral and central nervous system. Multiple sclerosis (MS) is the most common disease affecting the CNS white matter. Close similarities between MS and the animal model of the disease, Experimental Allergic Encephalitis (EAE), have suggested that MS might be an autoimmune disease, which istriggered by an infectiousagent. Our laboratory hasdirected its effort in identifying and designing therapies that interfere with key signaling pathways that mediate CNS inflammation in Experimental Allergic Encephalitis. These have included naturally occurring cytokines such as TGFβ and synthetic small molecules, lysofyline and tyrphostin, which inhibit the inflammatory response and prevent the development of EAE.
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Expression of IL-12 in CNS and lymphoid organs of mice with Experimental Allergic Encephalitis
Journal of neuroimmunology, 1998Co-Authors: John J. Bright, Bola F Musuro, Subramaniam SriramAbstract:Abstract EAE is a Th1 cell-mediated inflammatory autoimmune demyelinating disease of the central nervous system. IL-12 is a 70 kd heterodimeric cytokine, capable of regulating a wide range of immune functions. In view of its crucial role in the development of Th1 immune responses, we studied the expression of IL-12 p40 in the CNS and lymphoid organs of mice with EAE. RT-PCR analysis showed an increase in the expression of IL-12 p40 in brain and spinal cord during the acute paralytic phase of EAE and that decreased upon clinical recovery. The expression of p40 mRNA was also increased in spleen, lymph node and liver along with an elevated levels of circulating serum IL-12 during the height of disease. In vivo administration of rIL-12 increased the proliferative response and IFN- γ production of MBP sensitized T cells and that was decreased following treatment with anti-IL-12 antibody. The expression of IL-12 in the target and lymphoid organs of animals with EAE, the induction of a Th1 type immune response following immunization with neuronal antigens and the inhibition of clinical disease upon treatment with anti-IL-12 antibody, suggest the crucial role of IL-12 in the pathogenesis of EAE.
Francoise Lazarini - One of the best experts on this subject based on the ideXlab platform.
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role of the α chemokine stromal cell derived factor sdf 1 in the developing and mature central nervous system
Glia, 2003Co-Authors: Francoise Lazarini, To Nam Tham, Philippe Casanova, Fernando Arenzanaseisdedos, Monique DuboisdalcqAbstract:α-chemokines, which control the activation and directed migration of leukocytes, participate in the inflammatory processes in host defense response. One of the α-chemokines, CXCL12 or stromal cell-derived factor 1 (SDF-1), not only regulates cell growth and migration of hematopoietic stem cells but may also play a central role in brain development as we discuss here. SDF-1 indeed activates the CXCR4 receptor expressed in a variety of neural cells, and this signaling results in diverse biological effects. It enhances migration and proliferation of cerebellar granule cells, chemoattracts microglia, and stimulates cytokine production and glutamate release by astrocytes. Moreover, it elicits postsynaptic currents in Purkinje cells, triggers migration of cortical neuron progenitors, and produces pain by directly exciting nociceptive neurons. By modulating cell signaling and survival during neuroinflammation, SDF-1 may also play a role in the pathogenesis of brain tumors, Experimental Allergic Encephalitis, and the nervous system dysfunction associated with acquired immunodeficiency syndrome. GLIA 42:139–148, 2003. © 2003 Wiley-Liss, Inc.
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Role of the α-chemokine stromal cell-derived factor (SDF-1) in the developing and mature central nervous system
Glia, 2003Co-Authors: Francoise Lazarini, To Nam Tham, Philippe Casanova, Fernando Arenzana-seisdedos, Monique Dubois-dalcqAbstract:alpha-chemokines, which control the activation and directed migration of leukocytes, participate in the inflammatory processes in host defense response. One of the alpha-chemokines, CXCL12 or stromal cell-derived factor 1 (SDF-1), not only regulates cell growth and migration of hematopoietic stem cells but may also play a central role in brain development as we discuss here. SDF-1 indeed activates the CXCR4 receptor expressed in a variety of neural cells, and this signaling results in diverse biological effects. It enhances migration and proliferation of cerebellar granule cells, chemoattracts microglia, and stimulates cytokine production and glutamate release by astrocytes. Moreover, it elicits postsynaptic currents in Purkinje cells, triggers migration of cortical neuron progenitors, and produces pain by directly exciting nociceptive neurons. By modulating cell signaling and survival during neuroinflammation, SDF-1 may also play a role in the pathogenesis of brain tumors, Experimental Allergic Encephalitis, and the nervous system dysfunction associated with acquired immunodeficiency syndrome.
Monique Duboisdalcq - One of the best experts on this subject based on the ideXlab platform.
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role of the α chemokine stromal cell derived factor sdf 1 in the developing and mature central nervous system
Glia, 2003Co-Authors: Francoise Lazarini, To Nam Tham, Philippe Casanova, Fernando Arenzanaseisdedos, Monique DuboisdalcqAbstract:α-chemokines, which control the activation and directed migration of leukocytes, participate in the inflammatory processes in host defense response. One of the α-chemokines, CXCL12 or stromal cell-derived factor 1 (SDF-1), not only regulates cell growth and migration of hematopoietic stem cells but may also play a central role in brain development as we discuss here. SDF-1 indeed activates the CXCR4 receptor expressed in a variety of neural cells, and this signaling results in diverse biological effects. It enhances migration and proliferation of cerebellar granule cells, chemoattracts microglia, and stimulates cytokine production and glutamate release by astrocytes. Moreover, it elicits postsynaptic currents in Purkinje cells, triggers migration of cortical neuron progenitors, and produces pain by directly exciting nociceptive neurons. By modulating cell signaling and survival during neuroinflammation, SDF-1 may also play a role in the pathogenesis of brain tumors, Experimental Allergic Encephalitis, and the nervous system dysfunction associated with acquired immunodeficiency syndrome. GLIA 42:139–148, 2003. © 2003 Wiley-Liss, Inc.
Monique Dubois-dalcq - One of the best experts on this subject based on the ideXlab platform.
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Role of the α-chemokine stromal cell-derived factor (SDF-1) in the developing and mature central nervous system
Glia, 2003Co-Authors: Francoise Lazarini, To Nam Tham, Philippe Casanova, Fernando Arenzana-seisdedos, Monique Dubois-dalcqAbstract:alpha-chemokines, which control the activation and directed migration of leukocytes, participate in the inflammatory processes in host defense response. One of the alpha-chemokines, CXCL12 or stromal cell-derived factor 1 (SDF-1), not only regulates cell growth and migration of hematopoietic stem cells but may also play a central role in brain development as we discuss here. SDF-1 indeed activates the CXCR4 receptor expressed in a variety of neural cells, and this signaling results in diverse biological effects. It enhances migration and proliferation of cerebellar granule cells, chemoattracts microglia, and stimulates cytokine production and glutamate release by astrocytes. Moreover, it elicits postsynaptic currents in Purkinje cells, triggers migration of cortical neuron progenitors, and produces pain by directly exciting nociceptive neurons. By modulating cell signaling and survival during neuroinflammation, SDF-1 may also play a role in the pathogenesis of brain tumors, Experimental Allergic Encephalitis, and the nervous system dysfunction associated with acquired immunodeficiency syndrome.
Philippe Casanova - One of the best experts on this subject based on the ideXlab platform.
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role of the α chemokine stromal cell derived factor sdf 1 in the developing and mature central nervous system
Glia, 2003Co-Authors: Francoise Lazarini, To Nam Tham, Philippe Casanova, Fernando Arenzanaseisdedos, Monique DuboisdalcqAbstract:α-chemokines, which control the activation and directed migration of leukocytes, participate in the inflammatory processes in host defense response. One of the α-chemokines, CXCL12 or stromal cell-derived factor 1 (SDF-1), not only regulates cell growth and migration of hematopoietic stem cells but may also play a central role in brain development as we discuss here. SDF-1 indeed activates the CXCR4 receptor expressed in a variety of neural cells, and this signaling results in diverse biological effects. It enhances migration and proliferation of cerebellar granule cells, chemoattracts microglia, and stimulates cytokine production and glutamate release by astrocytes. Moreover, it elicits postsynaptic currents in Purkinje cells, triggers migration of cortical neuron progenitors, and produces pain by directly exciting nociceptive neurons. By modulating cell signaling and survival during neuroinflammation, SDF-1 may also play a role in the pathogenesis of brain tumors, Experimental Allergic Encephalitis, and the nervous system dysfunction associated with acquired immunodeficiency syndrome. GLIA 42:139–148, 2003. © 2003 Wiley-Liss, Inc.
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Role of the α-chemokine stromal cell-derived factor (SDF-1) in the developing and mature central nervous system
Glia, 2003Co-Authors: Francoise Lazarini, To Nam Tham, Philippe Casanova, Fernando Arenzana-seisdedos, Monique Dubois-dalcqAbstract:alpha-chemokines, which control the activation and directed migration of leukocytes, participate in the inflammatory processes in host defense response. One of the alpha-chemokines, CXCL12 or stromal cell-derived factor 1 (SDF-1), not only regulates cell growth and migration of hematopoietic stem cells but may also play a central role in brain development as we discuss here. SDF-1 indeed activates the CXCR4 receptor expressed in a variety of neural cells, and this signaling results in diverse biological effects. It enhances migration and proliferation of cerebellar granule cells, chemoattracts microglia, and stimulates cytokine production and glutamate release by astrocytes. Moreover, it elicits postsynaptic currents in Purkinje cells, triggers migration of cortical neuron progenitors, and produces pain by directly exciting nociceptive neurons. By modulating cell signaling and survival during neuroinflammation, SDF-1 may also play a role in the pathogenesis of brain tumors, Experimental Allergic Encephalitis, and the nervous system dysfunction associated with acquired immunodeficiency syndrome.
