Interleukin-6 via Toll-Like Receptor 3 Signaling Attenuates the Expression of Proinflammatory Chemokines in Human Podocytes
Background: Although toll-like receptor 3 (TLR3) signaling is involved in the development of certain chronic kidney diseases, the specific molecular mechanisms underlying inflammatory reactions via activation of TLR3 signaling in human podocytes remain unclear. Interleukin (IL)-6 is a pleiotropic cy...
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| Veröffentlicht in: | Kidney & blood pressure research 2021-04, Vol.46 (2), p.207-218 |
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| container_title | Kidney & blood pressure research |
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| creator | Umetsu, Hidenori Watanabe, Shojiro Imaizumi, Tadaatsu Aizawa, Tomomi Tsugawa, Koji Kawaguchi, Shogo Seya, Kazuhiko Matsumiya, Tomoh Tanaka, Hiroshi |
| description | Background: Although toll-like receptor 3 (TLR3) signaling is involved in the development of certain chronic kidney diseases, the specific molecular mechanisms underlying inflammatory reactions via activation of TLR3 signaling in human podocytes remain unclear. Interleukin (IL)-6 is a pleiotropic cytokine associated with innate and adaptive immune responses; however, little is known about the implication of IL-6 via the activation of regional TLR3 signaling in the inflammatory reactions in human podocytes. Methods: We treated immortalized human podocytes with polyinosinic-polycytidylic acid (poly IC), an authentic viral double-stranded RNA, and assessed the expression of IL-6, monocyte chemoattractant protein-1 (MCP-1), and C-C motif chemokine ligand 5 (CCL5) using quantitative real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. To further elucidate the poly IC-induced signaling pathway, we subjected the cells to RNA interference against IFN-β and IL-6. Results: We found that the activation of TLR3 induced expression of IL-6, MCP-1, CCL5, and IFN-β in human podocytes. RNA interference experiments revealed that IFN-β was involved in the poly IC-induced expression of IL-6, MCP-1, and CCL5. Interestingly, IL-6 knockdown markedly increased the poly IC-induced expression of MCP-1 and CCL5. Further, treatment of cells with IL-6 attenuated the expression of CCL5 and MCP-1 mRNA and proteins. Conclusion: IL-6 induced by TLR3 signaling negatively regulates the expression of representative TLR3 signaling-dependent proinflammatory chemokines in human podocytes. |
| doi_str_mv | 10.1159/000514589 |
| format | Article |
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Interleukin (IL)-6 is a pleiotropic cytokine associated with innate and adaptive immune responses; however, little is known about the implication of IL-6 via the activation of regional TLR3 signaling in the inflammatory reactions in human podocytes. Methods: We treated immortalized human podocytes with polyinosinic-polycytidylic acid (poly IC), an authentic viral double-stranded RNA, and assessed the expression of IL-6, monocyte chemoattractant protein-1 (MCP-1), and C-C motif chemokine ligand 5 (CCL5) using quantitative real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. To further elucidate the poly IC-induced signaling pathway, we subjected the cells to RNA interference against IFN-β and IL-6. Results: We found that the activation of TLR3 induced expression of IL-6, MCP-1, CCL5, and IFN-β in human podocytes. RNA interference experiments revealed that IFN-β was involved in the poly IC-induced expression of IL-6, MCP-1, and CCL5. Interestingly, IL-6 knockdown markedly increased the poly IC-induced expression of MCP-1 and CCL5. Further, treatment of cells with IL-6 attenuated the expression of CCL5 and MCP-1 mRNA and proteins. Conclusion: IL-6 induced by TLR3 signaling negatively regulates the expression of representative TLR3 signaling-dependent proinflammatory chemokines in human podocytes.</description><identifier>ISSN: 1420-4096</identifier><identifier>EISSN: 1423-0143</identifier><identifier>DOI: 10.1159/000514589</identifier><identifier>PMID: 33827102</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Adaptive immunity ; c-c motif chemokine ligand 5 ; Chemokines ; Cytokines ; Double-stranded RNA ; Enzyme-linked immunosorbent assay ; Experiments ; Gene expression ; Immune response ; Inflammation ; Interference ; Interleukin 6 ; Interleukins ; Kidney diseases ; Ligands ; Molecular modelling ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; Monocytes ; Pathogenesis ; podocytes ; Polyinosinic:polycytidylic acid ; Polymerase chain reaction ; Proteins ; Receptors ; Research Article ; Reverse transcription ; RNA-mediated interference ; Signal transduction ; Signaling ; Software ; Standard deviation ; TLR3 protein ; toll-like receptor 3 ; Toll-like receptors ; β-Interferon</subject><ispartof>Kidney & blood pressure research, 2021-04, Vol.46 (2), p.207-218</ispartof><rights>2021 The Author(s). Published by S. Karger AG, Basel</rights><rights>2021 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c641t-5d6b584d6558ca3dbc68c1272911d19e1f279535edd2d51591df87bd5ccaf3213</citedby><cites>FETCH-LOGICAL-c641t-5d6b584d6558ca3dbc68c1272911d19e1f279535edd2d51591df87bd5ccaf3213</cites><orcidid>0000-0001-5599-1110</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2096,27612,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33827102$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Umetsu, Hidenori</creatorcontrib><creatorcontrib>Watanabe, Shojiro</creatorcontrib><creatorcontrib>Imaizumi, Tadaatsu</creatorcontrib><creatorcontrib>Aizawa, Tomomi</creatorcontrib><creatorcontrib>Tsugawa, Koji</creatorcontrib><creatorcontrib>Kawaguchi, Shogo</creatorcontrib><creatorcontrib>Seya, Kazuhiko</creatorcontrib><creatorcontrib>Matsumiya, Tomoh</creatorcontrib><creatorcontrib>Tanaka, Hiroshi</creatorcontrib><title>Interleukin-6 via Toll-Like Receptor 3 Signaling Attenuates the Expression of Proinflammatory Chemokines in Human Podocytes</title><title>Kidney & blood pressure research</title><addtitle>Kidney Blood Press Res</addtitle><description>Background: Although toll-like receptor 3 (TLR3) signaling is involved in the development of certain chronic kidney diseases, the specific molecular mechanisms underlying inflammatory reactions via activation of TLR3 signaling in human podocytes remain unclear. Interleukin (IL)-6 is a pleiotropic cytokine associated with innate and adaptive immune responses; however, little is known about the implication of IL-6 via the activation of regional TLR3 signaling in the inflammatory reactions in human podocytes. Methods: We treated immortalized human podocytes with polyinosinic-polycytidylic acid (poly IC), an authentic viral double-stranded RNA, and assessed the expression of IL-6, monocyte chemoattractant protein-1 (MCP-1), and C-C motif chemokine ligand 5 (CCL5) using quantitative real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. To further elucidate the poly IC-induced signaling pathway, we subjected the cells to RNA interference against IFN-β and IL-6. Results: We found that the activation of TLR3 induced expression of IL-6, MCP-1, CCL5, and IFN-β in human podocytes. RNA interference experiments revealed that IFN-β was involved in the poly IC-induced expression of IL-6, MCP-1, and CCL5. Interestingly, IL-6 knockdown markedly increased the poly IC-induced expression of MCP-1 and CCL5. Further, treatment of cells with IL-6 attenuated the expression of CCL5 and MCP-1 mRNA and proteins. Conclusion: IL-6 induced by TLR3 signaling negatively regulates the expression of representative TLR3 signaling-dependent proinflammatory chemokines in human podocytes.</description><subject>Adaptive immunity</subject><subject>c-c motif chemokine ligand 5</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Double-stranded RNA</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Immune response</subject><subject>Inflammation</subject><subject>Interference</subject><subject>Interleukin 6</subject><subject>Interleukins</subject><subject>Kidney diseases</subject><subject>Ligands</subject><subject>Molecular modelling</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Pathogenesis</subject><subject>podocytes</subject><subject>Polyinosinic:polycytidylic acid</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Research Article</subject><subject>Reverse transcription</subject><subject>RNA-mediated interference</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Software</subject><subject>Standard deviation</subject><subject>TLR3 protein</subject><subject>toll-like receptor 3</subject><subject>Toll-like receptors</subject><subject>β-Interferon</subject><issn>1420-4096</issn><issn>1423-0143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptkU1vEzEQhlcIRD_gwB0hS1zKYcHf2T2WqNCISFSlnC2vPZs62bW39i4i4s_jNCFIiJMt65lnxu8UxSuC3xMi6g8YY0G4qOonxSnhlJWYcPb08Y5Ljmt5UpyltN5hGNPnxQljFZ0RTE-LXws_Quxg2jhfSvTDaXQXuq5cug2gWzAwjCEihr65lded8yt0OY7gJz1CQuM9oKufQ4SUXPAotOgmBufbTve9znVbNL-HPmR1hp1H11OvPboJNphtrn9RPGt1l-Dl4Twvvn-6uptfl8uvnxfzy2VpJCdjKaxsRMWtFKIymtnGyMoQOqM1IZbUQFo6qwUTYC21IudBbFvNGiuM0S2jhJ0Xi73XBr1WQ3S9jlsVtFOPDyGulI6jMx0obXENVDa0Bc1rw6vst1jWDca8oYZm18XeNcTwMEEaVe-Sga7THsKUFBU5VilnnGf07T_oOkwxp7ijOOMsf2hHvdtTJoaUIrTHAQlWu-2q43Yz--ZgnJoe7JH8s86_LTc6riAegS8fb_cKNdg2U6__Sx26_AYRIbOM</recordid><startdate>20210401</startdate><enddate>20210401</enddate><creator>Umetsu, Hidenori</creator><creator>Watanabe, Shojiro</creator><creator>Imaizumi, Tadaatsu</creator><creator>Aizawa, Tomomi</creator><creator>Tsugawa, Koji</creator><creator>Kawaguchi, Shogo</creator><creator>Seya, Kazuhiko</creator><creator>Matsumiya, Tomoh</creator><creator>Tanaka, Hiroshi</creator><general>S. 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3 Signaling Attenuates the Expression of Proinflammatory Chemokines in Human Podocytes</title><author>Umetsu, Hidenori ; Watanabe, Shojiro ; Imaizumi, Tadaatsu ; Aizawa, Tomomi ; Tsugawa, Koji ; Kawaguchi, Shogo ; Seya, Kazuhiko ; Matsumiya, Tomoh ; Tanaka, Hiroshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c641t-5d6b584d6558ca3dbc68c1272911d19e1f279535edd2d51591df87bd5ccaf3213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adaptive immunity</topic><topic>c-c motif chemokine ligand 5</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Double-stranded RNA</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>Immune response</topic><topic>Inflammation</topic><topic>Interference</topic><topic>Interleukin 6</topic><topic>Interleukins</topic><topic>Kidney diseases</topic><topic>Ligands</topic><topic>Molecular modelling</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Pathogenesis</topic><topic>podocytes</topic><topic>Polyinosinic:polycytidylic acid</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Receptors</topic><topic>Research Article</topic><topic>Reverse transcription</topic><topic>RNA-mediated interference</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Software</topic><topic>Standard deviation</topic><topic>TLR3 protein</topic><topic>toll-like receptor 3</topic><topic>Toll-like receptors</topic><topic>β-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Umetsu, Hidenori</creatorcontrib><creatorcontrib>Watanabe, Shojiro</creatorcontrib><creatorcontrib>Imaizumi, Tadaatsu</creatorcontrib><creatorcontrib>Aizawa, 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Tomoh</au><au>Tanaka, Hiroshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interleukin-6 via Toll-Like Receptor 3 Signaling Attenuates the Expression of Proinflammatory Chemokines in Human Podocytes</atitle><jtitle>Kidney & blood pressure research</jtitle><addtitle>Kidney Blood Press Res</addtitle><date>2021-04-01</date><risdate>2021</risdate><volume>46</volume><issue>2</issue><spage>207</spage><epage>218</epage><pages>207-218</pages><issn>1420-4096</issn><eissn>1423-0143</eissn><abstract>Background: Although toll-like receptor 3 (TLR3) signaling is involved in the development of certain chronic kidney diseases, the specific molecular mechanisms underlying inflammatory reactions via activation of TLR3 signaling in human podocytes remain unclear. Interleukin (IL)-6 is a pleiotropic cytokine associated with innate and adaptive immune responses; however, little is known about the implication of IL-6 via the activation of regional TLR3 signaling in the inflammatory reactions in human podocytes. Methods: We treated immortalized human podocytes with polyinosinic-polycytidylic acid (poly IC), an authentic viral double-stranded RNA, and assessed the expression of IL-6, monocyte chemoattractant protein-1 (MCP-1), and C-C motif chemokine ligand 5 (CCL5) using quantitative real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. To further elucidate the poly IC-induced signaling pathway, we subjected the cells to RNA interference against IFN-β and IL-6. Results: We found that the activation of TLR3 induced expression of IL-6, MCP-1, CCL5, and IFN-β in human podocytes. RNA interference experiments revealed that IFN-β was involved in the poly IC-induced expression of IL-6, MCP-1, and CCL5. Interestingly, IL-6 knockdown markedly increased the poly IC-induced expression of MCP-1 and CCL5. Further, treatment of cells with IL-6 attenuated the expression of CCL5 and MCP-1 mRNA and proteins. Conclusion: IL-6 induced by TLR3 signaling negatively regulates the expression of representative TLR3 signaling-dependent proinflammatory chemokines in human podocytes.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>33827102</pmid><doi>10.1159/000514589</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-5599-1110</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptive immunity c-c motif chemokine ligand 5 Chemokines Cytokines Double-stranded RNA Enzyme-linked immunosorbent assay Experiments Gene expression Immune response Inflammation Interference Interleukin 6 Interleukins Kidney diseases Ligands Molecular modelling Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Monocytes Pathogenesis podocytes Polyinosinic:polycytidylic acid Polymerase chain reaction Proteins Receptors Research Article Reverse transcription RNA-mediated interference Signal transduction Signaling Software Standard deviation TLR3 protein toll-like receptor 3 Toll-like receptors β-Interferon |
| title | Interleukin-6 via Toll-Like Receptor 3 Signaling Attenuates the Expression of Proinflammatory Chemokines in Human Podocytes |
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