NLRX1 does not inhibit MAVS-dependent antiviral signalling
NLRX1 is a member of the Nod-like receptor family of intracellular sensors of microbial- and danger-associated molecular patterns. NLRX1 has a N-terminal mitochondrial addressing sequence that localizes the protein to the mitochondrial matrix. Recently, conflicting reports have been presented with r...
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| Veröffentlicht in: | Innate immunity (London, England) England), 2013-08, Vol.19 (4), p.438-448 |
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| creator | Soares, Fraser Tattoli, Ivan Wortzman, Michael E Arnoult, Damien Philpott, Dana J Girardin, Stephen E |
| description | NLRX1 is a member of the Nod-like receptor family of intracellular sensors of microbial- and danger-associated molecular patterns. NLRX1 has a N-terminal mitochondrial addressing sequence that localizes the protein to the mitochondrial matrix. Recently, conflicting reports have been presented with regard to the putative implication of NLRX1 as a negative regulator of MAVS-dependent cytosolic antiviral responses. Here, we generated a new NLRX1 knockout mouse strain and observed that bone marrow-derived macrophages and murine embryonic fibroblasts from NLRX1-deficient mice displayed normal antiviral and inflammatory responses following Sendai virus infection. Importantly, wild type and NLRX1-deficient mice exhibited unaltered antiviral and inflammatory gene expression following intranasal challenge with influenza A virus or i.p. injection of Poly (I:C). Together, our results demonstrate that NLRX1 does not participate in the negative regulation of MAVS-dependent antiviral responses. |
| doi_str_mv | 10.1177/1753425912467383 |
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NLRX1 has a N-terminal mitochondrial addressing sequence that localizes the protein to the mitochondrial matrix. Recently, conflicting reports have been presented with regard to the putative implication of NLRX1 as a negative regulator of MAVS-dependent cytosolic antiviral responses. Here, we generated a new NLRX1 knockout mouse strain and observed that bone marrow-derived macrophages and murine embryonic fibroblasts from NLRX1-deficient mice displayed normal antiviral and inflammatory responses following Sendai virus infection. Importantly, wild type and NLRX1-deficient mice exhibited unaltered antiviral and inflammatory gene expression following intranasal challenge with influenza A virus or i.p. injection of Poly (I:C). 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NLRX1 has a N-terminal mitochondrial addressing sequence that localizes the protein to the mitochondrial matrix. Recently, conflicting reports have been presented with regard to the putative implication of NLRX1 as a negative regulator of MAVS-dependent cytosolic antiviral responses. Here, we generated a new NLRX1 knockout mouse strain and observed that bone marrow-derived macrophages and murine embryonic fibroblasts from NLRX1-deficient mice displayed normal antiviral and inflammatory responses following Sendai virus infection. Importantly, wild type and NLRX1-deficient mice exhibited unaltered antiviral and inflammatory gene expression following intranasal challenge with influenza A virus or i.p. injection of Poly (I:C). Together, our results demonstrate that NLRX1 does not participate in the negative regulation of MAVS-dependent antiviral responses.</description><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Animals</subject><subject>Cell Line</subject><subject>Chemokine CXCL10 - genetics</subject><subject>Chemokine CXCL10 - metabolism</subject><subject>Fibroblasts - immunology</subject><subject>Immunity, Innate</subject><subject>Inflammation Mediators - metabolism</subject><subject>Influenza A virus</subject><subject>Influenza A virus - immunology</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Macrophages - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Orthomyxoviridae Infections - immunology</subject><subject>Poly I-C - immunology</subject><subject>Respirovirus Infections - immunology</subject><subject>Sendai virus</subject><subject>Sendai virus - immunology</subject><subject>Signal Transduction</subject><issn>1753-4259</issn><issn>1753-4267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEtLw0AUhQdRbK3uXUmWbqIzd14dd6X4gqrgC3dhMnNbp6RJzSSC_96U1i4EwdU9XL5zFh8hx4yeMab1OdOSC5CGgVCaD_kO6a9eqQCld7dZmh45iHFOqQIq9T7pAQcGUrA-ubifPL6xxFcYk7JqklC-hzw0yd3o9Sn1uMTSY9kktmzCZ6htkcQwK21RhHJ2SPamtoh4tLkD8nJ1-Ty-SScP17fj0SR1QsgmZdw7UI5SY41VU6DaAEVlvTXKe50zcNJo5ZEbozjmesjB5UYJpE4BTvmAnK53l3X10WJsskWIDovClli1MWOCGa44B_UPdOUAJIcOpWvU1VWMNU6zZR0Wtv7KGM1WcrPfcrvKyWa9zRfot4Ufmx2QroFoZ5jNq7buVMW_B78Bq15-ww</recordid><startdate>20130801</startdate><enddate>20130801</enddate><creator>Soares, Fraser</creator><creator>Tattoli, Ivan</creator><creator>Wortzman, Michael E</creator><creator>Arnoult, Damien</creator><creator>Philpott, Dana J</creator><creator>Girardin, Stephen E</creator><general>SAGE Publications</general><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>7X8</scope><scope>7T5</scope><scope>7T7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>20130801</creationdate><title>NLRX1 does not inhibit MAVS-dependent antiviral signalling</title><author>Soares, Fraser ; 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NLRX1 has a N-terminal mitochondrial addressing sequence that localizes the protein to the mitochondrial matrix. Recently, conflicting reports have been presented with regard to the putative implication of NLRX1 as a negative regulator of MAVS-dependent cytosolic antiviral responses. Here, we generated a new NLRX1 knockout mouse strain and observed that bone marrow-derived macrophages and murine embryonic fibroblasts from NLRX1-deficient mice displayed normal antiviral and inflammatory responses following Sendai virus infection. Importantly, wild type and NLRX1-deficient mice exhibited unaltered antiviral and inflammatory gene expression following intranasal challenge with influenza A virus or i.p. injection of Poly (I:C). 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| subjects | Adaptor Proteins, Signal Transducing - metabolism Animals Cell Line Chemokine CXCL10 - genetics Chemokine CXCL10 - metabolism Fibroblasts - immunology Immunity, Innate Inflammation Mediators - metabolism Influenza A virus Influenza A virus - immunology Interleukin-6 - genetics Interleukin-6 - metabolism Macrophages - immunology Mice Mice, Inbred C57BL Mice, Knockout Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism Orthomyxoviridae Infections - immunology Poly I-C - immunology Respirovirus Infections - immunology Sendai virus Sendai virus - immunology Signal Transduction |
| title | NLRX1 does not inhibit MAVS-dependent antiviral signalling |
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