The Experts below are selected from a list of 399 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.
Asa Ljunggren-rose - 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.
Song-yi Yao - One of the best experts on this subject based on the ideXlab platform.
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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.
Hilary Koprowski - One of the best experts on this subject based on the ideXlab platform.
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Local nitric oxide production in viral and autoimmune diseases of the central nervous system.
Proceedings of the National Academy of Sciences of the United States of America, 1995Co-Authors: Douglas Craig Hooper, Bernhard Dietzschold, S T Ohnishi, Rhonda B. Kean, Y Numagami, Hilary KoprowskiAbstract:Because of the short half-life of NO, previous studies implicating NO in central nervous system pathology during infection had to rely on the demonstration of elevated levels of NO synthase mRNA or enzyme expression or NO metabolites such as nitrate and nitrite in the infected brain. To more definitively investigate the potential causative role of NO in lesions of the central nervous system in animals infected with neurotropic viruses or suffering from experimental Allergic Encephalitis, we have determined directly the levels of NO present in the central nervous system of such animals. Using spin trapping of NO and electron paramagnetic resonance spectroscopy, we confirm here that copious amounts of NO (up to 30-fold more than control) are elaborated in the brains of rats infected with rabies virus or borna disease virus, as well as in the spinal cords of rats that had received myelin basic protein-specific T cells.
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In vivo expression of inducible nitric oxide synthase in experimentally induced neurologic diseases
Proceedings of the National Academy of Sciences of the United States of America, 1993Co-Authors: Hilary Koprowski, Yong Mu Zheng, Ellen Heber-katz, Nigel W. Fraser, Lucy B. Rorke, Cathleen A. Hanlon, Bernhard DietzscholdAbstract:The purpose of this study was to investigate the induction of inducible nitric oxide synthase (iNOS) mRNA in the brain tissue of rats and mice under the following experimental conditions: in rats infected with borna disease virus and rabies virus, in mice infected with herpes simplex virus, and in rats after the induction of experimental Allergic Encephalitis. The results showed that iNOS mRNA, normally nondetectable in the brain, was present in animals after viral infection or after induction of experimental Allergic Encephalitis. The induction of iNOS mRNA coincided with the severity of clinical signs and in some cases with the presence of inflammatory cells in the brain. The results indicate that nitric oxide produced by cells induced by iNOS may be the toxic factor accounting for cell damage and this may open the door to approaches to the study of the pathogenesis of neurological diseases.
Dennis L Kasper - One of the best experts on this subject based on the ideXlab platform.
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the starting lineup key microbial players in intestinal immunity and homeostasis
Frontiers in Microbiology, 2011Co-Authors: Nicola C Reading, Dennis L KasperAbstract:The complexity of microbiota inhabiting the intestine is increasingly apparent. Delicate balance of numerous bacterial species can affect development of the immune system, how susceptible a host is to pathogenic organisms, and the auto-inflammatory state of the host. In the last decade, with the increased use of germ-free mice, gnotobiotic mice, and animal models in which a germ-free animal has been colonized with a foreign microbiota such as humanized mice, it has been possible to delineate relationships that specific bacteria have with the host immune system and to show what role they may play in overall host health. These models have not only allowed us to tease out the role of each individual species, but have also allowed the discovery and characterization of functionally unknown organisms. For example, Segmented Filamentous Bacteria (SFB) have been shown to play a vital role in expansion of IL-17 producing cells. Prior to linking their key role in immune system development, little was known about these organisms. Bacteroides fragilis can rescue some of the immune defects of gnotobiotic mice after mono-colonization and have anti-inflammatory properties that can alleviate colitis and experimental Allergic Encephalitis in murine models. Additionally, Clostridium species have most recently been shown to expand regulatory T-cell populations leading to anti-inflammatory conditions. This review will highlight and summarize some of the major findings within the last decade concerning the role of select groups of bacteria including SFB, Clostridium, Bacteroides, Bifidobacterium, and Lactobacillis, and their impact on host mucosal immune systems.