Expression and Functional Characterization of Retinoic Acid-Inducible Gene-I-Like Receptors of Mast Cells in Response to Viral Infection
To investigate the precise mechanisms of virus recognition by mast cells, the expression and functional characteristics of virus recognition receptors that lead to mast cell activation were investigated. Our results suggest that mast cells are partly responsible for the early in vivo production of a...
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Veröffentlicht in: | Journal of innate immunity 2013-01, Vol.5 (2), p.163-173 |
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creator | Fukuda, Minoru Ushio, Hiroko Kawasaki, Junko Niyonsaba, Francois Takeuchi, Mizuho Baba, Tadashi Hiramatsu, Keiichi Okumura, Ko Ogawa, Hideoki |
description | To investigate the precise mechanisms of virus recognition by mast cells, the expression and functional characteristics of virus recognition receptors that lead to mast cell activation were investigated. Our results suggest that mast cells are partly responsible for the early in vivo production of antiviral cytokines and chemokines upon vesicular stomatitis virus (VSV) infection. Analysis of the expression of double-stranded RNA (dsRNA) recognition receptors in murine bone marrow-derived mast cells (BMMCs) revealed that BMMCs express melanoma differentiation-associated gene 5 (MDA5), protein kinase RNA-activated, retinoic acid-inducible gene-I (RIG-I) and Toll-like receptor 3. The expression levels of these receptors were found to increase upon stimulation of mast cells with VSV as well as synthetic dsRNA: polyinosinic-polycytidylic acid. Moreover, small interfering RNA analysis to identify the receptors responsible for mast cell activation by VSV revealed that both RIG-I and MDA5 were involved in cytokine production but not in the degranulation of mast cells. Our findings suggest that mast cells produce cytokines and chemokines in the early infection stage after recognizing viruses via RIG-I and MDA5, and may contribute to antiviral responses. These data provide additional novel information that improves our understanding of antiviral innate responses that involve mast cells. |
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Our results suggest that mast cells are partly responsible for the early in vivo production of antiviral cytokines and chemokines upon vesicular stomatitis virus (VSV) infection. Analysis of the expression of double-stranded RNA (dsRNA) recognition receptors in murine bone marrow-derived mast cells (BMMCs) revealed that BMMCs express melanoma differentiation-associated gene 5 (MDA5), protein kinase RNA-activated, retinoic acid-inducible gene-I (RIG-I) and Toll-like receptor 3. The expression levels of these receptors were found to increase upon stimulation of mast cells with VSV as well as synthetic dsRNA: polyinosinic-polycytidylic acid. Moreover, small interfering RNA analysis to identify the receptors responsible for mast cell activation by VSV revealed that both RIG-I and MDA5 were involved in cytokine production but not in the degranulation of mast cells. Our findings suggest that mast cells produce cytokines and chemokines in the early infection stage after recognizing viruses via RIG-I and MDA5, and may contribute to antiviral responses. These data provide additional novel information that improves our understanding of antiviral innate responses that involve mast cells.</description><identifier>ISSN: 1662-811X</identifier><identifier>EISSN: 1662-8128</identifier><identifier>DOI: 10.1159/000343895</identifier><identifier>PMID: 23171655</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Bone Marrow - immunology ; Cell Degranulation - genetics ; Cell Degranulation - immunology ; Cells, Cultured ; Cytokines - metabolism ; DEAD-box RNA Helicases - genetics ; DEAD-box RNA Helicases - metabolism ; Gene Expression Regulation ; Immunity, Innate - genetics ; Interferon-Induced Helicase, IFIH1 ; Mast Cells - immunology ; Mast Cells - virology ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Research Article ; RNA, Small Interfering - genetics ; RNA, Viral - immunology ; Toll-Like Receptor 3 - genetics ; Toll-Like Receptor 3 - metabolism ; Vesicular Stomatitis - immunology ; Vesiculovirus - immunology</subject><ispartof>Journal of innate immunity, 2013-01, Vol.5 (2), p.163-173</ispartof><rights>2012 S. Karger AG, Basel</rights><rights>Copyright © 2012 S. Karger AG, Basel.</rights><rights>Copyright (c) 2013 S. Karger AG, Basel</rights><rights>Copyright © 2012 by S. Karger AG, Basel 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c518t-e8dcb12ec5c5d24025c171114fb8417d221799d637c2fc17e2246707de30f0583</citedby><cites>FETCH-LOGICAL-c518t-e8dcb12ec5c5d24025c171114fb8417d221799d637c2fc17e2246707de30f0583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6784038/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6784038/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23171655$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fukuda, Minoru</creatorcontrib><creatorcontrib>Ushio, Hiroko</creatorcontrib><creatorcontrib>Kawasaki, Junko</creatorcontrib><creatorcontrib>Niyonsaba, Francois</creatorcontrib><creatorcontrib>Takeuchi, Mizuho</creatorcontrib><creatorcontrib>Baba, Tadashi</creatorcontrib><creatorcontrib>Hiramatsu, Keiichi</creatorcontrib><creatorcontrib>Okumura, Ko</creatorcontrib><creatorcontrib>Ogawa, Hideoki</creatorcontrib><title>Expression and Functional Characterization of Retinoic Acid-Inducible Gene-I-Like Receptors of Mast Cells in Response to Viral Infection</title><title>Journal of innate immunity</title><addtitle>J Innate Immun</addtitle><description>To investigate the precise mechanisms of virus recognition by mast cells, the expression and functional characteristics of virus recognition receptors that lead to mast cell activation were investigated. Our results suggest that mast cells are partly responsible for the early in vivo production of antiviral cytokines and chemokines upon vesicular stomatitis virus (VSV) infection. Analysis of the expression of double-stranded RNA (dsRNA) recognition receptors in murine bone marrow-derived mast cells (BMMCs) revealed that BMMCs express melanoma differentiation-associated gene 5 (MDA5), protein kinase RNA-activated, retinoic acid-inducible gene-I (RIG-I) and Toll-like receptor 3. The expression levels of these receptors were found to increase upon stimulation of mast cells with VSV as well as synthetic dsRNA: polyinosinic-polycytidylic acid. Moreover, small interfering RNA analysis to identify the receptors responsible for mast cell activation by VSV revealed that both RIG-I and MDA5 were involved in cytokine production but not in the degranulation of mast cells. Our findings suggest that mast cells produce cytokines and chemokines in the early infection stage after recognizing viruses via RIG-I and MDA5, and may contribute to antiviral responses. These data provide additional novel information that improves our understanding of antiviral innate responses that involve mast cells.</description><subject>Animals</subject><subject>Bone Marrow - immunology</subject><subject>Cell Degranulation - genetics</subject><subject>Cell Degranulation - immunology</subject><subject>Cells, Cultured</subject><subject>Cytokines - metabolism</subject><subject>DEAD-box RNA Helicases - genetics</subject><subject>DEAD-box RNA Helicases - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Immunity, Innate - genetics</subject><subject>Interferon-Induced Helicase, IFIH1</subject><subject>Mast Cells - immunology</subject><subject>Mast Cells - virology</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Research Article</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA, Viral - immunology</subject><subject>Toll-Like Receptor 3 - genetics</subject><subject>Toll-Like Receptor 3 - metabolism</subject><subject>Vesicular Stomatitis - immunology</subject><subject>Vesiculovirus - immunology</subject><issn>1662-811X</issn><issn>1662-8128</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkUtv1DAUhSNERUthwR4hS2xgEfAzTjZI1aiPoAEkBIid5bFvWrcZO9gJAn4BPxuHGcJDrPw4n8-517coHhD8jBDRPMcYM87qRtwqjkhV0bImtL697MnHw-JuStcYV5w38k5xSBmRpBLiqPh--mWIkJILHmlv0dnkzZgPukerKx21GSG6b3q-QqFDb2F0PjiDToyzZevtZNymB3QOHsq2XLsbyIyBYQwxzQ9e6TSiFfR9Qs5nKQ3BJ0BjQB9czCGt7-Bn4L3ioNN9gvv79bh4f3b6bnVRrt-ct6uTdWkEqccSams2hIIRRljKMRUmt0II7zY1J9JSSmTT2IpJQ7ssAaW8klhaYLjDombHxYud7zBttmAN-DHXoYbotjp-VUE79bfi3ZW6DJ9VJWuO2WzwZG8Qw6cJ0qi2LpncofYQpqQIo0w2FSZNRh__g16HKea_nSneUIqZwJl6uqNMDClF6JZiCFbzfNUy38w--rP6hfw10N-RNzpeQlyAl-3rnYUabJeph_-l9ik_AH2BtaM</recordid><startdate>20130101</startdate><enddate>20130101</enddate><creator>Fukuda, Minoru</creator><creator>Ushio, Hiroko</creator><creator>Kawasaki, Junko</creator><creator>Niyonsaba, Francois</creator><creator>Takeuchi, Mizuho</creator><creator>Baba, Tadashi</creator><creator>Hiramatsu, Keiichi</creator><creator>Okumura, Ko</creator><creator>Ogawa, Hideoki</creator><general>S. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of innate immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fukuda, Minoru</au><au>Ushio, Hiroko</au><au>Kawasaki, Junko</au><au>Niyonsaba, Francois</au><au>Takeuchi, Mizuho</au><au>Baba, Tadashi</au><au>Hiramatsu, Keiichi</au><au>Okumura, Ko</au><au>Ogawa, Hideoki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression and Functional Characterization of Retinoic Acid-Inducible Gene-I-Like Receptors of Mast Cells in Response to Viral Infection</atitle><jtitle>Journal of innate immunity</jtitle><addtitle>J Innate Immun</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>5</volume><issue>2</issue><spage>163</spage><epage>173</epage><pages>163-173</pages><issn>1662-811X</issn><eissn>1662-8128</eissn><abstract>To investigate the precise mechanisms of virus recognition by mast cells, the expression and functional characteristics of virus recognition receptors that lead to mast cell activation were investigated. Our results suggest that mast cells are partly responsible for the early in vivo production of antiviral cytokines and chemokines upon vesicular stomatitis virus (VSV) infection. Analysis of the expression of double-stranded RNA (dsRNA) recognition receptors in murine bone marrow-derived mast cells (BMMCs) revealed that BMMCs express melanoma differentiation-associated gene 5 (MDA5), protein kinase RNA-activated, retinoic acid-inducible gene-I (RIG-I) and Toll-like receptor 3. The expression levels of these receptors were found to increase upon stimulation of mast cells with VSV as well as synthetic dsRNA: polyinosinic-polycytidylic acid. Moreover, small interfering RNA analysis to identify the receptors responsible for mast cell activation by VSV revealed that both RIG-I and MDA5 were involved in cytokine production but not in the degranulation of mast cells. Our findings suggest that mast cells produce cytokines and chemokines in the early infection stage after recognizing viruses via RIG-I and MDA5, and may contribute to antiviral responses. These data provide additional novel information that improves our understanding of antiviral innate responses that involve mast cells.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>23171655</pmid><doi>10.1159/000343895</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Bone Marrow - immunology Cell Degranulation - genetics Cell Degranulation - immunology Cells, Cultured Cytokines - metabolism DEAD-box RNA Helicases - genetics DEAD-box RNA Helicases - metabolism Gene Expression Regulation Immunity, Innate - genetics Interferon-Induced Helicase, IFIH1 Mast Cells - immunology Mast Cells - virology Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mice, Knockout Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Research Article RNA, Small Interfering - genetics RNA, Viral - immunology Toll-Like Receptor 3 - genetics Toll-Like Receptor 3 - metabolism Vesicular Stomatitis - immunology Vesiculovirus - immunology |
title | Expression and Functional Characterization of Retinoic Acid-Inducible Gene-I-Like Receptors of Mast Cells in Response to Viral Infection |
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