The mitochondrial and kidney disease phenotypes of kd/kd mice under germfree conditions
Interstitial nephritis occurs spontaneously in kd/kd mice, but the mechanisms leading to this disease have not been fully elucidated. The earliest manifestation of a phenotype is the appearance of ultrastructural defects in the mitochondria of mice as young as 42 days of age. To examine the influenc...
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| Veröffentlicht in: | Journal of autoimmunity 2006-02, Vol.26 (1), p.1-6 |
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| creator | Hallman, Troy M. Peng, Min Meade, Ray Hancock, Wayne W. Madaio, Michael P. Gasser, David L. |
| description | Interstitial nephritis occurs spontaneously in
kd/kd mice, but the mechanisms leading to this disease have not been fully elucidated. The earliest manifestation of a phenotype is the appearance of ultrastructural defects in the mitochondria of mice as young as 42
days of age. To examine the influence of the environment on the phenotype, homozygous B6.
kd/kd mice were transferred from specific pathogen-free (SPF) conditions to a germfree (GF) environment, and the development of the disease was observed. The GF state resulted in a highly significant reduction in the frequency of tubulointerstitial nephritis. In addition, GF conditions markedly reduced the appearance of the mitochondrial phenotype, with no sign of mitochondrial abnormalities in GF mice of up to 155
days of age. These results suggest that environmental factors are involved in the progression of all known manifestations of this disease phenotype. |
| doi_str_mv | 10.1016/j.jaut.2005.10.006 |
| format | Article |
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kd/kd mice, but the mechanisms leading to this disease have not been fully elucidated. The earliest manifestation of a phenotype is the appearance of ultrastructural defects in the mitochondria of mice as young as 42
days of age. To examine the influence of the environment on the phenotype, homozygous B6.
kd/kd mice were transferred from specific pathogen-free (SPF) conditions to a germfree (GF) environment, and the development of the disease was observed. The GF state resulted in a highly significant reduction in the frequency of tubulointerstitial nephritis. In addition, GF conditions markedly reduced the appearance of the mitochondrial phenotype, with no sign of mitochondrial abnormalities in GF mice of up to 155
days of age. These results suggest that environmental factors are involved in the progression of all known manifestations of this disease phenotype.</description><identifier>ISSN: 0896-8411</identifier><identifier>EISSN: 1095-9157</identifier><identifier>DOI: 10.1016/j.jaut.2005.10.006</identifier><identifier>PMID: 16337774</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Animals ; Autoimmunity ; Biological and medical sciences ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; General aspects ; Germ-Free Life ; Germfree ; Immunopathology ; Kidney - pathology ; Kidney - ultrastructure ; Kidney disease ; Medical sciences ; Mice ; Mice, Mutant Strains ; Mitochondria ; Mitochondria - ultrastructure ; Nephritis, Interstitial - etiology ; Nephritis, Interstitial - immunology ; Nephritis, Interstitial - pathology ; Phenotype ; Specific Pathogen-Free Organisms</subject><ispartof>Journal of autoimmunity, 2006-02, Vol.26 (1), p.1-6</ispartof><rights>2005 Elsevier Ltd</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-5c86290284042e930e1e84ee08983beb9709c001a80ddb9b140e8f175875dfd83</citedby><cites>FETCH-LOGICAL-c514t-5c86290284042e930e1e84ee08983beb9709c001a80ddb9b140e8f175875dfd83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0896841105001423$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17471280$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16337774$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hallman, Troy M.</creatorcontrib><creatorcontrib>Peng, Min</creatorcontrib><creatorcontrib>Meade, Ray</creatorcontrib><creatorcontrib>Hancock, Wayne W.</creatorcontrib><creatorcontrib>Madaio, Michael P.</creatorcontrib><creatorcontrib>Gasser, David L.</creatorcontrib><title>The mitochondrial and kidney disease phenotypes of kd/kd mice under germfree conditions</title><title>Journal of autoimmunity</title><addtitle>J Autoimmun</addtitle><description>Interstitial nephritis occurs spontaneously in
kd/kd mice, but the mechanisms leading to this disease have not been fully elucidated. The earliest manifestation of a phenotype is the appearance of ultrastructural defects in the mitochondria of mice as young as 42
days of age. To examine the influence of the environment on the phenotype, homozygous B6.
kd/kd mice were transferred from specific pathogen-free (SPF) conditions to a germfree (GF) environment, and the development of the disease was observed. The GF state resulted in a highly significant reduction in the frequency of tubulointerstitial nephritis. In addition, GF conditions markedly reduced the appearance of the mitochondrial phenotype, with no sign of mitochondrial abnormalities in GF mice of up to 155
days of age. These results suggest that environmental factors are involved in the progression of all known manifestations of this disease phenotype.</description><subject>Animals</subject><subject>Autoimmunity</subject><subject>Biological and medical sciences</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>General aspects</subject><subject>Germ-Free Life</subject><subject>Germfree</subject><subject>Immunopathology</subject><subject>Kidney - pathology</subject><subject>Kidney - ultrastructure</subject><subject>Kidney disease</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Mitochondria</subject><subject>Mitochondria - ultrastructure</subject><subject>Nephritis, Interstitial - etiology</subject><subject>Nephritis, Interstitial - immunology</subject><subject>Nephritis, Interstitial - pathology</subject><subject>Phenotype</subject><subject>Specific Pathogen-Free Organisms</subject><issn>0896-8411</issn><issn>1095-9157</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2KFDEUhYMoTjv6Ai4kG91VT5JKKgmIMAz-wYCbEZchldyaTnd10iZVA_32pujG0Y2uLtz7ncNJDkKvKVlTQrur7Xpr52nNCBF1sSake4JWlGjRaCrkU7QiSneN4pReoBelbAmhVAjxHF3Qrm2llHyFftxtAO_DlNwmRZ-DHbGNHu-Cj3DEPhSwBfBhAzFNxwMUnAa881c7X0UO8Bw9ZHwPeT9kAOyqR5hCiuUlejbYscCr87xE3z99vLv50tx--_z15vq2cYLyqRFOdUwTpjjhDHRLgILiADW5anvotSTa1dxWEe973VNOQA1UCiWFH7xqL9GHk-9h7vfgHcQp29EcctjbfDTJBvP3JYaNuU8PhjHBGWPV4N3ZIKefM5TJ7ENxMI42QpqLkaTTgjLxX5BKSrimSyR2Al1OpWQYfqehxCzFma1ZijNLccuuFldFb_58x6Pk3FQF3p4BW5wdh2yjC-WRk1xSpkjl3p84qL_-ECCb4gJEBz5kcJPxKfwrxy__xbe9</recordid><startdate>20060201</startdate><enddate>20060201</enddate><creator>Hallman, Troy M.</creator><creator>Peng, Min</creator><creator>Meade, Ray</creator><creator>Hancock, Wayne W.</creator><creator>Madaio, Michael P.</creator><creator>Gasser, David L.</creator><general>Elsevier Ltd</general><general>Elsevier</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>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060201</creationdate><title>The mitochondrial and kidney disease phenotypes of kd/kd mice under germfree conditions</title><author>Hallman, Troy M. ; Peng, Min ; Meade, Ray ; Hancock, Wayne W. ; Madaio, Michael P. ; Gasser, David L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-5c86290284042e930e1e84ee08983beb9709c001a80ddb9b140e8f175875dfd83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Autoimmunity</topic><topic>Biological and medical sciences</topic><topic>Fundamental and applied biological sciences. 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kd/kd mice, but the mechanisms leading to this disease have not been fully elucidated. The earliest manifestation of a phenotype is the appearance of ultrastructural defects in the mitochondria of mice as young as 42
days of age. To examine the influence of the environment on the phenotype, homozygous B6.
kd/kd mice were transferred from specific pathogen-free (SPF) conditions to a germfree (GF) environment, and the development of the disease was observed. The GF state resulted in a highly significant reduction in the frequency of tubulointerstitial nephritis. In addition, GF conditions markedly reduced the appearance of the mitochondrial phenotype, with no sign of mitochondrial abnormalities in GF mice of up to 155
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| subjects | Animals Autoimmunity Biological and medical sciences Fundamental and applied biological sciences. Psychology Fundamental immunology General aspects Germ-Free Life Germfree Immunopathology Kidney - pathology Kidney - ultrastructure Kidney disease Medical sciences Mice Mice, Mutant Strains Mitochondria Mitochondria - ultrastructure Nephritis, Interstitial - etiology Nephritis, Interstitial - immunology Nephritis, Interstitial - pathology Phenotype Specific Pathogen-Free Organisms |
| title | The mitochondrial and kidney disease phenotypes of kd/kd mice under germfree conditions |
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