Effects of neutralizing antibodies on cytokine treatment for anti-GBM nephritis in mouse
The process of glomerular injury in nephrotoxic serum nephritis (NTN) is dependent on proinflammatory cytokines. In the present investigation, we assessed the actions of neutralizing antibody against IL-1, 9, TNF-α, IL-6 and TGF-β1 on glomerular injury. Marked increase in IL-1 and IL-6 was detected...
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| Veröffentlicht in: | Nihon Jinzo Gakkai shi 1996, Vol.38(12), pp.563-570 |
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| container_issue | 12 |
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| container_title | Nihon Jinzo Gakkai shi |
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| creator | HATTORI, Tomohisa FUJITSUKA, Naoki KUROGI, Akiko SHINDO, Shoichiro |
| description | The process of glomerular injury in nephrotoxic serum nephritis (NTN) is dependent on proinflammatory cytokines. In the present investigation, we assessed the actions of neutralizing antibody against IL-1, 9, TNF-α, IL-6 and TGF-β1 on glomerular injury. Marked increase in IL-1 and IL-6 was detected in cultured glomeruli of NTN in mice throughout the experiments from disease induction. Protein of TNF-α and TGF-$1 also increased in NTN mice 1 day after disease induction. Treatment with either IL-l, S or TNF- a neutralizing antibody reduced proteinuria from 71 ± 11.2 m g/24 hr to 32.2±6.0 (P |
| doi_str_mv | 10.14842/jpnjnephrol1959.38.563 |
| format | Article |
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In the present investigation, we assessed the actions of neutralizing antibody against IL-1, 9, TNF-α, IL-6 and TGF-β1 on glomerular injury. Marked increase in IL-1 and IL-6 was detected in cultured glomeruli of NTN in mice throughout the experiments from disease induction. Protein of TNF-α and TGF-$1 also increased in NTN mice 1 day after disease induction. Treatment with either IL-l, S or TNF- a neutralizing antibody reduced proteinuria from 71 ± 11.2 m g/24 hr to 32.2±6.0 (P<0.01), 34.3±6.8 mg/24 hr (P<0.01), respectively. Although the effect of IL-6 neutralizing antibody on proteinuria was not remarkable, the decreased creatinine clearance was improved more than that of IL-1 βor TNF-α. Antibody against TGF-β 1 had no effect on proteinuria and creatinine clearance. Treatments with IL-1 β, TNF-α and IL-6 neutralizing antibodies inhibited glomerular hypercellularity in NTN mice. TGF-β1 neutralizing antibody suppressed the index of mesangial matrix expansion. IL-l, 3 and TNF-αneutralizing antibodies prevented the increase in the number of macrophages in the glomeruli. The number of PCNA positive cells and alpha;-smooth muscle actin expression in glomeruli was significantly reduced in the IL-6 neutralizing antibody-treated group. These results confirm the direct involvement of IL-1β, TNF-αand IL-6 in mouse NTN. We speculate that TGF-β1 may inhibit excessive proliferation in glomerular cells.</description><identifier>ISSN: 0385-2385</identifier><identifier>EISSN: 1884-0728</identifier><identifier>DOI: 10.14842/jpnjnephrol1959.38.563</identifier><identifier>PMID: 9014475</identifier><language>jpn</language><publisher>Japan: Japanese Society of Nephrology</publisher><subject>Animals ; Anti-GBM nephritis, Interleukin-1β, TNF-α, Interleukin-6 ; Antibodies - immunology ; Autoantibodies ; Cytokines - immunology ; Glomerulonephritis - immunology ; Glomerulonephritis - pathology ; Interleukin-1 - immunology ; Interleukin-6 - immunology ; Kidney Glomerulus - immunology ; Mice ; Mice, Inbred BALB C ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>The Japanese Journal of Nephrology, 1996, Vol.38(12), pp.563-570</ispartof><rights>Japanese Society of Nephrology</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9014475$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HATTORI, Tomohisa</creatorcontrib><creatorcontrib>FUJITSUKA, Naoki</creatorcontrib><creatorcontrib>KUROGI, Akiko</creatorcontrib><creatorcontrib>SHINDO, Shoichiro</creatorcontrib><title>Effects of neutralizing antibodies on cytokine treatment for anti-GBM nephritis in mouse</title><title>Nihon Jinzo Gakkai shi</title><addtitle>Jpn J Nephrol</addtitle><description>The process of glomerular injury in nephrotoxic serum nephritis (NTN) is dependent on proinflammatory cytokines. In the present investigation, we assessed the actions of neutralizing antibody against IL-1, 9, TNF-α, IL-6 and TGF-β1 on glomerular injury. Marked increase in IL-1 and IL-6 was detected in cultured glomeruli of NTN in mice throughout the experiments from disease induction. Protein of TNF-α and TGF-$1 also increased in NTN mice 1 day after disease induction. Treatment with either IL-l, S or TNF- a neutralizing antibody reduced proteinuria from 71 ± 11.2 m g/24 hr to 32.2±6.0 (P<0.01), 34.3±6.8 mg/24 hr (P<0.01), respectively. Although the effect of IL-6 neutralizing antibody on proteinuria was not remarkable, the decreased creatinine clearance was improved more than that of IL-1 βor TNF-α. Antibody against TGF-β 1 had no effect on proteinuria and creatinine clearance. Treatments with IL-1 β, TNF-α and IL-6 neutralizing antibodies inhibited glomerular hypercellularity in NTN mice. TGF-β1 neutralizing antibody suppressed the index of mesangial matrix expansion. IL-l, 3 and TNF-αneutralizing antibodies prevented the increase in the number of macrophages in the glomeruli. The number of PCNA positive cells and alpha;-smooth muscle actin expression in glomeruli was significantly reduced in the IL-6 neutralizing antibody-treated group. These results confirm the direct involvement of IL-1β, TNF-αand IL-6 in mouse NTN. We speculate that TGF-β1 may inhibit excessive proliferation in glomerular cells.</description><subject>Animals</subject><subject>Anti-GBM nephritis, Interleukin-1β, TNF-α, Interleukin-6</subject><subject>Antibodies - immunology</subject><subject>Autoantibodies</subject><subject>Cytokines - immunology</subject><subject>Glomerulonephritis - immunology</subject><subject>Glomerulonephritis - pathology</subject><subject>Interleukin-1 - immunology</subject><subject>Interleukin-6 - immunology</subject><subject>Kidney Glomerulus - immunology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><issn>0385-2385</issn><issn>1884-0728</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkM1OwzAQhC0EKlXpIyD8Ain-S2wfoSoFqRUXkLhFTrJuHRKnctxDeXpCW_XAZfbwjUY7g9ADJTMqlGCP9c7XHnbb0DVUp3rG1SzN-BUaU6VEQiRT12hMuEoTNsgtmva9KwhVkvBUihEaaUKFkOkYfS2shTL2uLPYwz4G07gf5zfY-OiKrnIwII_LQ-y-nQccA5jYgo_YduFoSpbPa3x8xkXXY-dx2-17uEM31jQ9TM93gj5fFh_z12T1vnybP62SmgkVE2Ep41JkoGXBqCmF5VLKDEATToRWkKWUAFSiqORQVWTaMvvXzBaZLqjlE3R_yt3tixaqfBdca8IhPzcc-PrE6z6aDVy4CdGVDeT_psy5yik767DpxVduTcjB81-lBXNx</recordid><startdate>1996</startdate><enddate>1996</enddate><creator>HATTORI, Tomohisa</creator><creator>FUJITSUKA, Naoki</creator><creator>KUROGI, Akiko</creator><creator>SHINDO, Shoichiro</creator><general>Japanese Society of Nephrology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>1996</creationdate><title>Effects of neutralizing antibodies on cytokine treatment for anti-GBM nephritis in mouse</title><author>HATTORI, Tomohisa ; FUJITSUKA, Naoki ; KUROGI, Akiko ; SHINDO, Shoichiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j248t-4f123746e97b21ac4f37776ee9030498e6510eed4bd7195469f2f0385fb69b1f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>jpn</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Anti-GBM nephritis, Interleukin-1β, TNF-α, Interleukin-6</topic><topic>Antibodies - immunology</topic><topic>Autoantibodies</topic><topic>Cytokines - immunology</topic><topic>Glomerulonephritis - immunology</topic><topic>Glomerulonephritis - pathology</topic><topic>Interleukin-1 - immunology</topic><topic>Interleukin-6 - immunology</topic><topic>Kidney Glomerulus - immunology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><toplevel>online_resources</toplevel><creatorcontrib>HATTORI, Tomohisa</creatorcontrib><creatorcontrib>FUJITSUKA, Naoki</creatorcontrib><creatorcontrib>KUROGI, Akiko</creatorcontrib><creatorcontrib>SHINDO, Shoichiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Nihon Jinzo Gakkai shi</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HATTORI, Tomohisa</au><au>FUJITSUKA, Naoki</au><au>KUROGI, Akiko</au><au>SHINDO, Shoichiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of neutralizing antibodies on cytokine treatment for anti-GBM nephritis in mouse</atitle><jtitle>Nihon Jinzo Gakkai shi</jtitle><addtitle>Jpn J Nephrol</addtitle><date>1996</date><risdate>1996</risdate><volume>38</volume><issue>12</issue><spage>563</spage><epage>570</epage><pages>563-570</pages><issn>0385-2385</issn><eissn>1884-0728</eissn><abstract>The process of glomerular injury in nephrotoxic serum nephritis (NTN) is dependent on proinflammatory cytokines. In the present investigation, we assessed the actions of neutralizing antibody against IL-1, 9, TNF-α, IL-6 and TGF-β1 on glomerular injury. Marked increase in IL-1 and IL-6 was detected in cultured glomeruli of NTN in mice throughout the experiments from disease induction. Protein of TNF-α and TGF-$1 also increased in NTN mice 1 day after disease induction. Treatment with either IL-l, S or TNF- a neutralizing antibody reduced proteinuria from 71 ± 11.2 m g/24 hr to 32.2±6.0 (P<0.01), 34.3±6.8 mg/24 hr (P<0.01), respectively. Although the effect of IL-6 neutralizing antibody on proteinuria was not remarkable, the decreased creatinine clearance was improved more than that of IL-1 βor TNF-α. Antibody against TGF-β 1 had no effect on proteinuria and creatinine clearance. Treatments with IL-1 β, TNF-α and IL-6 neutralizing antibodies inhibited glomerular hypercellularity in NTN mice. TGF-β1 neutralizing antibody suppressed the index of mesangial matrix expansion. IL-l, 3 and TNF-αneutralizing antibodies prevented the increase in the number of macrophages in the glomeruli. The number of PCNA positive cells and alpha;-smooth muscle actin expression in glomeruli was significantly reduced in the IL-6 neutralizing antibody-treated group. These results confirm the direct involvement of IL-1β, TNF-αand IL-6 in mouse NTN. We speculate that TGF-β1 may inhibit excessive proliferation in glomerular cells.</abstract><cop>Japan</cop><pub>Japanese Society of Nephrology</pub><pmid>9014475</pmid><doi>10.14842/jpnjnephrol1959.38.563</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0385-2385 |
| ispartof | The Japanese Journal of Nephrology, 1996, Vol.38(12), pp.563-570 |
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| subjects | Animals Anti-GBM nephritis, Interleukin-1β, TNF-α, Interleukin-6 Antibodies - immunology Autoantibodies Cytokines - immunology Glomerulonephritis - immunology Glomerulonephritis - pathology Interleukin-1 - immunology Interleukin-6 - immunology Kidney Glomerulus - immunology Mice Mice, Inbred BALB C Tumor Necrosis Factor-alpha - immunology |
| title | Effects of neutralizing antibodies on cytokine treatment for anti-GBM nephritis in mouse |
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