Myeloid differentiation factor-88 plays a crucial role in the pathogenesis of coxsackievirus B3-induced myocarditis and influences type I interferon production
Myeloid differentiation factor (MyD)-88 is a key adaptor protein that plays a major role in the innate immune pathway. How MyD88 may regulate host response in inflammatory heart disease is unknown. We found that the cardiac protein level of MyD88 was significantly increased in the hearts of wild-typ...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2005-10, Vol.112 (15), p.2276-2285 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | FUSE, Koichi CHAN, Grace YOUAN LIU GUDGEON, Patrick HUSAIN, Mansoor MANYIN CHEN YEH, Wen-Chen AKIRA, Shizuo LIU, Peter P |
| description | Myeloid differentiation factor (MyD)-88 is a key adaptor protein that plays a major role in the innate immune pathway. How MyD88 may regulate host response in inflammatory heart disease is unknown.
We found that the cardiac protein level of MyD88 was significantly increased in the hearts of wild-type mice after exposure to Coxsackievirus B3 (CVB3). MyD88(-/-) mice showed a dramatic higher survival rate (86%) in contrast to the low survival (35%) in the MyD88(+/+) mice after CVB3 infection (P |
| doi_str_mv | 10.1161/CIRCULATIONAHA.105.536433 |
| format | Article |
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We found that the cardiac protein level of MyD88 was significantly increased in the hearts of wild-type mice after exposure to Coxsackievirus B3 (CVB3). MyD88(-/-) mice showed a dramatic higher survival rate (86%) in contrast to the low survival (35%) in the MyD88(+/+) mice after CVB3 infection (P<0.0001). Pathological examination showed a significant decrease of cardiac and pancreatic inflammation in the MyD88(-/-) mice. Viral concentrations in the hearts were significantly decreased in the MyD88(-/-) mice. Cardiac mRNA levels for interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and IL-18 were significantly decreased in the MyD88(-/-) mice. Similarly, serum levels of T-helper 1 cytokines were significantly decreased in the MyD88(-/-) mice. In contrast, cardiac protein levels of the activated interferon regulatory factor (IRF)-3 and IFN-beta were significantly increased in the MyD88(-/-) mice but not other usual upstream signals to IRF-3. The cardiac expression of coxsackie-adenoviral receptor and p56(lck) were also significantly decreased.
MyD88 appears to be a key contributor to cardiac inflammation, mediating cytokine production and T-helper-1/2 cytokine balance, increasing coxsackie-adenoviral receptor and p56(lck) expression and viral titers after CVB3 exposure. Absence of MyD88 confers host protection possibly through novel direct activation of IRF-3 and IFN-beta.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/CIRCULATIONAHA.105.536433</identifier><identifier>PMID: 16216974</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adaptor Proteins, Signal Transducing - deficiency ; Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - physiology ; Animals ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Coronary heart disease ; Coxsackievirus B3 ; Disease Models, Animal ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; DNA Primers ; Drug toxicity and drugs side effects treatment ; Enterovirus B, Human ; Enterovirus Infections - complications ; Enterovirus Infections - immunology ; Heart ; Heart - virology ; HeLa Cells ; Humans ; Immunity, Innate ; Inflammation - immunology ; Inflammation - physiopathology ; Interferon Type I - biosynthesis ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Differentiation Factor 88 ; Myocarditis - immunology ; Myocarditis - physiopathology ; Myocarditis - virology ; Pharmacology. Drug treatments ; Reverse Transcriptase Polymerase Chain Reaction ; Toxicity: blood</subject><ispartof>Circulation (New York, N.Y.), 2005-10, Vol.112 (15), p.2276-2285</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c536t-ef6ac2aadc1ce5e23c396d882f2899472e798881a3c3d21535731579a0306b693</citedby><cites>FETCH-LOGICAL-c536t-ef6ac2aadc1ce5e23c396d882f2899472e798881a3c3d21535731579a0306b693</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3673,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17195701$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16216974$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FUSE, Koichi</creatorcontrib><creatorcontrib>CHAN, Grace</creatorcontrib><creatorcontrib>YOUAN LIU</creatorcontrib><creatorcontrib>GUDGEON, Patrick</creatorcontrib><creatorcontrib>HUSAIN, Mansoor</creatorcontrib><creatorcontrib>MANYIN CHEN</creatorcontrib><creatorcontrib>YEH, Wen-Chen</creatorcontrib><creatorcontrib>AKIRA, Shizuo</creatorcontrib><creatorcontrib>LIU, Peter P</creatorcontrib><title>Myeloid differentiation factor-88 plays a crucial role in the pathogenesis of coxsackievirus B3-induced myocarditis and influences type I interferon production</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Myeloid differentiation factor (MyD)-88 is a key adaptor protein that plays a major role in the innate immune pathway. How MyD88 may regulate host response in inflammatory heart disease is unknown.
We found that the cardiac protein level of MyD88 was significantly increased in the hearts of wild-type mice after exposure to Coxsackievirus B3 (CVB3). MyD88(-/-) mice showed a dramatic higher survival rate (86%) in contrast to the low survival (35%) in the MyD88(+/+) mice after CVB3 infection (P<0.0001). Pathological examination showed a significant decrease of cardiac and pancreatic inflammation in the MyD88(-/-) mice. Viral concentrations in the hearts were significantly decreased in the MyD88(-/-) mice. Cardiac mRNA levels for interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and IL-18 were significantly decreased in the MyD88(-/-) mice. Similarly, serum levels of T-helper 1 cytokines were significantly decreased in the MyD88(-/-) mice. In contrast, cardiac protein levels of the activated interferon regulatory factor (IRF)-3 and IFN-beta were significantly increased in the MyD88(-/-) mice but not other usual upstream signals to IRF-3. The cardiac expression of coxsackie-adenoviral receptor and p56(lck) were also significantly decreased.
MyD88 appears to be a key contributor to cardiac inflammation, mediating cytokine production and T-helper-1/2 cytokine balance, increasing coxsackie-adenoviral receptor and p56(lck) expression and viral titers after CVB3 exposure. Absence of MyD88 confers host protection possibly through novel direct activation of IRF-3 and IFN-beta.</description><subject>Adaptor Proteins, Signal Transducing - deficiency</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - physiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Coxsackievirus B3</subject><subject>Disease Models, Animal</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>DNA Primers</subject><subject>Drug toxicity and drugs side effects treatment</subject><subject>Enterovirus B, Human</subject><subject>Enterovirus Infections - complications</subject><subject>Enterovirus Infections - immunology</subject><subject>Heart</subject><subject>Heart - virology</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Inflammation - immunology</subject><subject>Inflammation - physiopathology</subject><subject>Interferon Type I - biosynthesis</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myeloid Differentiation Factor 88</subject><subject>Myocarditis - immunology</subject><subject>Myocarditis - physiopathology</subject><subject>Myocarditis - virology</subject><subject>Pharmacology. Drug treatments</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Toxicity: blood</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhS0EokPhFZBZwC5DbMd_y2FU2pEGKqF2Hbn2NTVk4mA7FXkaXhVXM1LFipXle79zz7UPQu9IuyZEkI_b3bft7X5zs7v-urnarEnL15yJjrFnaEU47ZqOM_0crdq21Y1klJ6hVzn_qFfBJH-JzoigRGjZrdCfLwsMMTjsgveQYCzBlBBH7I0tMTVK4WkwS8YG2zTbYAac4gA4jLjcA55MuY_fYYQcMo4e2_g7G_szwENIc8afWBNGN1tw-LBEa5ILpYJmdHWAH2YYLWRclgnwrlYKpLpDNZ9SrKrHPV6jF94MGd6cznN0-_niZnvV7K8vd9vNvrH15aUBL4ylxjhLLHCgzDItnFLUU6V1JylIrZQipjYcJZxxyQiX2rSsFXdCs3P04Ti3Wv-aIZf-ELKFYTAjxDn3QglFZf2__4FEV05LWUF9BG2KOSfw_ZTCwaSlJ23_GGP_b4y1zPtjjFX79mQy3x3APSlPuVXg_Qkw2ZrBJzPakJ84STSXLWF_Adlvqkw</recordid><startdate>20051011</startdate><enddate>20051011</enddate><creator>FUSE, Koichi</creator><creator>CHAN, Grace</creator><creator>YOUAN LIU</creator><creator>GUDGEON, Patrick</creator><creator>HUSAIN, Mansoor</creator><creator>MANYIN CHEN</creator><creator>YEH, Wen-Chen</creator><creator>AKIRA, Shizuo</creator><creator>LIU, Peter P</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20051011</creationdate><title>Myeloid differentiation factor-88 plays a crucial role in the pathogenesis of coxsackievirus B3-induced myocarditis and influences type I interferon production</title><author>FUSE, Koichi ; CHAN, Grace ; YOUAN LIU ; GUDGEON, Patrick ; HUSAIN, Mansoor ; MANYIN CHEN ; YEH, Wen-Chen ; AKIRA, Shizuo ; LIU, Peter P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c536t-ef6ac2aadc1ce5e23c396d882f2899472e798881a3c3d21535731579a0306b693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adaptor Proteins, Signal Transducing - deficiency</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - physiology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Coxsackievirus B3</topic><topic>Disease Models, Animal</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>DNA Primers</topic><topic>Drug toxicity and drugs side effects treatment</topic><topic>Enterovirus B, Human</topic><topic>Enterovirus Infections - complications</topic><topic>Enterovirus Infections - immunology</topic><topic>Heart</topic><topic>Heart - virology</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>Immunity, Innate</topic><topic>Inflammation - immunology</topic><topic>Inflammation - physiopathology</topic><topic>Interferon Type I - biosynthesis</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myeloid Differentiation Factor 88</topic><topic>Myocarditis - immunology</topic><topic>Myocarditis - physiopathology</topic><topic>Myocarditis - virology</topic><topic>Pharmacology. Drug treatments</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Toxicity: blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FUSE, Koichi</creatorcontrib><creatorcontrib>CHAN, Grace</creatorcontrib><creatorcontrib>YOUAN LIU</creatorcontrib><creatorcontrib>GUDGEON, Patrick</creatorcontrib><creatorcontrib>HUSAIN, Mansoor</creatorcontrib><creatorcontrib>MANYIN CHEN</creatorcontrib><creatorcontrib>YEH, Wen-Chen</creatorcontrib><creatorcontrib>AKIRA, Shizuo</creatorcontrib><creatorcontrib>LIU, Peter P</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FUSE, Koichi</au><au>CHAN, Grace</au><au>YOUAN LIU</au><au>GUDGEON, Patrick</au><au>HUSAIN, Mansoor</au><au>MANYIN CHEN</au><au>YEH, Wen-Chen</au><au>AKIRA, Shizuo</au><au>LIU, Peter P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myeloid differentiation factor-88 plays a crucial role in the pathogenesis of coxsackievirus B3-induced myocarditis and influences type I interferon production</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2005-10-11</date><risdate>2005</risdate><volume>112</volume><issue>15</issue><spage>2276</spage><epage>2285</epage><pages>2276-2285</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Myeloid differentiation factor (MyD)-88 is a key adaptor protein that plays a major role in the innate immune pathway. How MyD88 may regulate host response in inflammatory heart disease is unknown.
We found that the cardiac protein level of MyD88 was significantly increased in the hearts of wild-type mice after exposure to Coxsackievirus B3 (CVB3). MyD88(-/-) mice showed a dramatic higher survival rate (86%) in contrast to the low survival (35%) in the MyD88(+/+) mice after CVB3 infection (P<0.0001). Pathological examination showed a significant decrease of cardiac and pancreatic inflammation in the MyD88(-/-) mice. Viral concentrations in the hearts were significantly decreased in the MyD88(-/-) mice. Cardiac mRNA levels for interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and IL-18 were significantly decreased in the MyD88(-/-) mice. Similarly, serum levels of T-helper 1 cytokines were significantly decreased in the MyD88(-/-) mice. In contrast, cardiac protein levels of the activated interferon regulatory factor (IRF)-3 and IFN-beta were significantly increased in the MyD88(-/-) mice but not other usual upstream signals to IRF-3. The cardiac expression of coxsackie-adenoviral receptor and p56(lck) were also significantly decreased.
MyD88 appears to be a key contributor to cardiac inflammation, mediating cytokine production and T-helper-1/2 cytokine balance, increasing coxsackie-adenoviral receptor and p56(lck) expression and viral titers after CVB3 exposure. Absence of MyD88 confers host protection possibly through novel direct activation of IRF-3 and IFN-beta.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>16216974</pmid><doi>10.1161/CIRCULATIONAHA.105.536433</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2005-10, Vol.112 (15), p.2276-2285 |
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| subjects | Adaptor Proteins, Signal Transducing - deficiency Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - physiology Animals Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Coronary heart disease Coxsackievirus B3 Disease Models, Animal Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous DNA Primers Drug toxicity and drugs side effects treatment Enterovirus B, Human Enterovirus Infections - complications Enterovirus Infections - immunology Heart Heart - virology HeLa Cells Humans Immunity, Innate Inflammation - immunology Inflammation - physiopathology Interferon Type I - biosynthesis Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Myeloid Differentiation Factor 88 Myocarditis - immunology Myocarditis - physiopathology Myocarditis - virology Pharmacology. Drug treatments Reverse Transcriptase Polymerase Chain Reaction Toxicity: blood |
| title | Myeloid differentiation factor-88 plays a crucial role in the pathogenesis of coxsackievirus B3-induced myocarditis and influences type I interferon production |
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