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10.1177/1759091415592126 http://scihub22266oqcxt.onion/10.1177/1759091415592126 C4552224!4552224 !26148848     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26148848 &cmd=llinks): Failed to open stream: HTTP request failed! 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Epigenetic Modulation of Microglial Inflammatory Gene Loci in Helminth-Induced Immune Suppression: Implications for Immune Regulation in Neurocysticercosis |pdf=|usr=}}{{26148848 }} gab.com Text Epigenetic Modulation of Microglial Inflammatory Gene Loci in Helminth-Induced Immune Suppression: Implications for Immune Regulation in Neurocysticercosis JO: ASN Neuro http://www.kidney.de/pget.php?&tw=1&pmid=26148848 #FOAvip In neurocysticercosis, parasite-induced immune suppressive effects are thought to play an important role in enabling site-specific inhibition of inflammatory responses to infections. It is axiomatic that microglia-mediated (M1 proinflammatory) response causes central nervous system inflammation; however, the mechanisms by which helminth parasites modulate microglia activation remain poorly understood. Here, we show that microglia display a diminished expression of M1-inflammatory mediators such as tumor necrosis factor-alpha (TNF-?), interleukin-6 (IL-6), and nitric oxide synthase 2 (NOS2) in murine neurocysticercosis. Microglia also exhibited a lack of myeloid cell maturation marker major histocompatibility complex (MHC)-II in these parasite-infected brains. Treatment of microglia with helminth soluble/secreted factors (HSFs) in vitro did not induce expression of M1-inflammatory signature molecule NOS2 as well as MHC-II in primary microglia. However, HSF treatment completely inhibited lipopolysaccharide-induced increase in expression of MHC-II, NOS2 and nitric oxide production in these cells. As epigenetic modulation of chromatin states that regulates recruitment of RNA polymerase II (Pol-II) is a key regulatory step in determining gene expression and functional outcome, we next evaluated whether HSF induced modulation of these phenomenon in microglia in vitro. Indeed, HSF downregulated Pol-II recruitment to the promoter region of TNF-?, IL-6, NOS2, MHC-II, and transcription factor CIITA (a regulator of MHC-II expression), by itself. Moreover, HSF suppressed the lipopolysaccharide-induced increase in Pol-II recruitment as well. In addition, HSF exposure reduced the positive histone marks H3K4Me3 and H3K9/14Ac at the promoter of TNF-?, IL-6, NOS2, MHC-II, and CIITA. These studies provide a novel mechanistic insight into helminth-mediated immune suppression in microglia via modulation of epigenetic processes. Twit Text FOAVip Epigenetic Modulation of Microglial Inflammatory Gene Loci in Helminth-Induced Immune Suppression: Implications for Immune Regulation in Neurocysticercosis ????ASN Neuro http://www.kidney.de/pget.php?&tw=1&pmid=26148848 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26148848 #FOAvip English Wikipedia <ref>{{Cite pmid|26148848 }}</ref> Epigenetic Modulation of Microglial Inflammatory Gene Loci in Helminth-Induced Immune Suppression: Implications for Immune Regulation in Neurocysticercosis #MMPMID26148848 Chauhan A ; Quenum FZ ; Abbas A ; Bradley DS ; Nechaev S ; Singh BB ; Sharma J ; Mishra BB ASN Neuro 2015[Jul]; 7 (4 ): ä PMID26148848 show ga In neurocysticercosis, parasite-induced immune suppressive effects are thought to play an important role in enabling site-specific inhibition of inflammatory responses to infections. It is axiomatic that microglia-mediated (M1 proinflammatory) response causes central nervous system inflammation; however, the mechanisms by which helminth parasites modulate microglia activation remain poorly understood. Here, we show that microglia display a diminished expression of M1-inflammatory mediators such as tumor necrosis factor-alpha (TNF-?), interleukin-6 (IL-6), and nitric oxide synthase 2 (NOS2) in murine neurocysticercosis. Microglia also exhibited a lack of myeloid cell maturation marker major histocompatibility complex (MHC)-II in these parasite-infected brains. Treatment of microglia with helminth soluble/secreted factors (HSFs) in vitro did not induce expression of M1-inflammatory signature molecule NOS2 as well as MHC-II in primary microglia. However, HSF treatment completely inhibited lipopolysaccharide-induced increase in expression of MHC-II, NOS2 and nitric oxide production in these cells. As epigenetic modulation of chromatin states that regulates recruitment of RNA polymerase II (Pol-II) is a key regulatory step in determining gene expression and functional outcome, we next evaluated whether HSF induced modulation of these phenomenon in microglia in vitro. Indeed, HSF downregulated Pol-II recruitment to the promoter region of TNF-?, IL-6, NOS2, MHC-II, and transcription factor CIITA (a regulator of MHC-II expression), by itself. Moreover, HSF suppressed the lipopolysaccharide-induced increase in Pol-II recruitment as well. In addition, HSF exposure reduced the positive histone marks H3K4Me3 and H3K9/14Ac at the promoter of TNF-?, IL-6, NOS2, MHC-II, and CIITA. These studies provide a novel mechanistic insight into helminth-mediated immune suppression in microglia via modulation of epigenetic processes. |Animals [MESH] |Animals, Newborn [MESH] |Cells, Cultured [MESH] |Central Nervous System/*pathology [MESH] |Chromatin Immunoprecipitation [MESH] |Cytokines/genetics/metabolism [MESH] |Disease Models, Animal [MESH] |Epigenesis, Genetic/drug effects/*immunology [MESH] |Helminthiasis/*immunology/*pathology [MESH] |Helminths/metabolism/*pathogenicity [MESH] |Histocompatibility Antigens Class II/genetics/metabolism [MESH] |Histones/genetics/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Microglia/drug effects/*metabolism [MESH] |Nitric Oxide Synthase Type II/genetics/metabolism [MESH] |Nuclear Proteins/genetics/metabolism [MESH] |Polysaccharides/pharmacology [MESH] |RNA Polymerase II/genetics/metabolism [MESH]Epigenetic Modulation of Microglial Inflammatory Gene Loci in Helminth(epmc).pdf DeepDyve Pubget Overpricing