Protective Effect of Antagonist of High-mobility Group Box 1 on Lipopolysaccharide-Induced Acute Lung Injury in Mice
We explored the effects of recombinant A-box (rA-box), a specific blockade for endogenous high mobility group box 1 (HMGB1) protein, on acute lung inflammation induced by lipopolysaccharide (LPS) in vivo. Acute lung injury (ALI) was produced successfully by intratracheal administration of LPS (10 μg...
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| Veröffentlicht in: | Scandinavian journal of immunology 2009, Vol.69 (1), p.29-35 |
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| creator | Gong, Q Xu, J.-F Yin, H Liu, S.-F Duan, L.-H Bian, Z.-L |
| description | We explored the effects of recombinant A-box (rA-box), a specific blockade for endogenous high mobility group box 1 (HMGB1) protein, on acute lung inflammation induced by lipopolysaccharide (LPS) in vivo. Acute lung injury (ALI) was produced successfully by intratracheal administration of LPS (10 μg/mouse) in male BALB/c mice. rA-box (0.3, 0.6 mg/mouse, i.p.) was administered 30 min prior to or 2 h after LPS exposure. Bronchoalveolar lavage fluid (BALF) was obtained to measure chemokines, proinflammatory cytokines, total cell counts and proteins at the indicated time points. It was found that rA-box caused a significant reduction in the total cells and neutrophils in BALF, a significant reduction in the W/D ratio and protein leakage at 24 h after LPS challenge. In addition, rA-box was also believed to have downregulated the expression of LPS-induced chemokines (keratinocyte-derived chemokine) and proinflammatory cytokines, including early mediator TNF-a and late mediator HMGB1. These findings confirm the significant protection of rA-box against LPS-induced ALI, and the effect mechanism of rA-box was associated with decreasing the expression of chemokines and proinflammatory cytokines. |
| doi_str_mv | 10.1111/j.1365-3083.2008.02194.x |
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Acute lung injury (ALI) was produced successfully by intratracheal administration of LPS (10 μg/mouse) in male BALB/c mice. rA-box (0.3, 0.6 mg/mouse, i.p.) was administered 30 min prior to or 2 h after LPS exposure. Bronchoalveolar lavage fluid (BALF) was obtained to measure chemokines, proinflammatory cytokines, total cell counts and proteins at the indicated time points. It was found that rA-box caused a significant reduction in the total cells and neutrophils in BALF, a significant reduction in the W/D ratio and protein leakage at 24 h after LPS challenge. In addition, rA-box was also believed to have downregulated the expression of LPS-induced chemokines (keratinocyte-derived chemokine) and proinflammatory cytokines, including early mediator TNF-a and late mediator HMGB1. These findings confirm the significant protection of rA-box against LPS-induced ALI, and the effect mechanism of rA-box was associated with decreasing the expression of chemokines and proinflammatory cytokines.</description><identifier>ISSN: 0300-9475</identifier><identifier>EISSN: 1365-3083</identifier><identifier>DOI: 10.1111/j.1365-3083.2008.02194.x</identifier><identifier>PMID: 19140874</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Acute Lung Injury - chemically induced ; Acute Lung Injury - immunology ; Acute Lung Injury - prevention & control ; Amino Acid Motifs ; Animals ; Bronchoalveolar Lavage Fluid - immunology ; Chemokines - metabolism ; Down-Regulation - drug effects ; HMGB1 Protein - antagonists & inhibitors ; Inflammation Mediators - metabolism ; Injections, Intraperitoneal ; Lipopolysaccharides - immunology ; Male ; Mice ; Mice, Inbred BALB C ; Recombinant Proteins - administration & dosage ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Scandinavian journal of immunology, 2009, Vol.69 (1), p.29-35</ispartof><rights>2009 The Authors. Journal compilation © 2009 Blackwell Publishing Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4224-6a5ac4412c261c5b614c182ce0bf1b608b2507d7da3c1bcc49e8cd1719ba0373</citedby><cites>FETCH-LOGICAL-c4224-6a5ac4412c261c5b614c182ce0bf1b608b2507d7da3c1bcc49e8cd1719ba0373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-3083.2008.02194.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-3083.2008.02194.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,4024,27923,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19140874$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gong, Q</creatorcontrib><creatorcontrib>Xu, J.-F</creatorcontrib><creatorcontrib>Yin, H</creatorcontrib><creatorcontrib>Liu, S.-F</creatorcontrib><creatorcontrib>Duan, L.-H</creatorcontrib><creatorcontrib>Bian, Z.-L</creatorcontrib><title>Protective Effect of Antagonist of High-mobility Group Box 1 on Lipopolysaccharide-Induced Acute Lung Injury in Mice</title><title>Scandinavian journal of immunology</title><addtitle>Scand J Immunol</addtitle><description>We explored the effects of recombinant A-box (rA-box), a specific blockade for endogenous high mobility group box 1 (HMGB1) protein, on acute lung inflammation induced by lipopolysaccharide (LPS) in vivo. Acute lung injury (ALI) was produced successfully by intratracheal administration of LPS (10 μg/mouse) in male BALB/c mice. rA-box (0.3, 0.6 mg/mouse, i.p.) was administered 30 min prior to or 2 h after LPS exposure. Bronchoalveolar lavage fluid (BALF) was obtained to measure chemokines, proinflammatory cytokines, total cell counts and proteins at the indicated time points. It was found that rA-box caused a significant reduction in the total cells and neutrophils in BALF, a significant reduction in the W/D ratio and protein leakage at 24 h after LPS challenge. In addition, rA-box was also believed to have downregulated the expression of LPS-induced chemokines (keratinocyte-derived chemokine) and proinflammatory cytokines, including early mediator TNF-a and late mediator HMGB1. These findings confirm the significant protection of rA-box against LPS-induced ALI, and the effect mechanism of rA-box was associated with decreasing the expression of chemokines and proinflammatory cytokines.</description><subject>Acute Lung Injury - chemically induced</subject><subject>Acute Lung Injury - immunology</subject><subject>Acute Lung Injury - prevention & control</subject><subject>Amino Acid Motifs</subject><subject>Animals</subject><subject>Bronchoalveolar Lavage Fluid - immunology</subject><subject>Chemokines - metabolism</subject><subject>Down-Regulation - drug effects</subject><subject>HMGB1 Protein - antagonists & inhibitors</subject><subject>Inflammation Mediators - metabolism</subject><subject>Injections, Intraperitoneal</subject><subject>Lipopolysaccharides - immunology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Recombinant Proteins - administration & dosage</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0300-9475</issn><issn>1365-3083</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcGO0zAQhi0EYkvhFcAnbgkzthMnBw5ltewWFYG0y9lyHKfrKo2DnUDz9iTbCq7MZWY0_z8jfUMIRUhxjg-HFHmeJRwKnjKAIgWGpUhPz8jq7-A5WQEHSEohsyvyKsYDAHIm-UtyhSUKKKRYkeF78IM1g_tl6U3TzBX1Dd10g977zsWn7s7tH5Ojr1zrhoneBj_29JM_UaS-ozvX-963U9TGPOrgaptsu3o0tqYbMw6W7sZuT7fdYQwTdR396ox9TV40uo32zSWvycPnm4fru2T37XZ7vdklRjAmklxn2giBzLAcTVblKAwWzFioGqxyKCqWgaxlrbnByhhR2sLUKLGsNHDJ1-T9eW0f_M_RxkEdXTS2bXVn_RgVAyYznFGtSXEWmuBjDLZRfXBHHSaFoBbg6qAWrmrhqhbg6gm4Os3Wt5cbY3W09T_jhfAs-HgW_Hatnf57sbr_sl2q2f_u7G-0V3ofXFQ_7tn8ScBMIuMF_wMGrJg7</recordid><startdate>2009</startdate><enddate>2009</enddate><creator>Gong, Q</creator><creator>Xu, J.-F</creator><creator>Yin, H</creator><creator>Liu, S.-F</creator><creator>Duan, L.-H</creator><creator>Bian, Z.-L</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><scope>FBQ</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></search><sort><creationdate>2009</creationdate><title>Protective Effect of Antagonist of High-mobility Group Box 1 on Lipopolysaccharide-Induced Acute Lung Injury in Mice</title><author>Gong, Q ; Xu, J.-F ; Yin, H ; Liu, S.-F ; Duan, L.-H ; Bian, Z.-L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4224-6a5ac4412c261c5b614c182ce0bf1b608b2507d7da3c1bcc49e8cd1719ba0373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Acute Lung Injury - chemically induced</topic><topic>Acute Lung Injury - immunology</topic><topic>Acute Lung Injury - prevention & control</topic><topic>Amino Acid Motifs</topic><topic>Animals</topic><topic>Bronchoalveolar Lavage Fluid - immunology</topic><topic>Chemokines - metabolism</topic><topic>Down-Regulation - drug effects</topic><topic>HMGB1 Protein - antagonists & inhibitors</topic><topic>Inflammation Mediators - metabolism</topic><topic>Injections, Intraperitoneal</topic><topic>Lipopolysaccharides - immunology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Recombinant Proteins - administration & dosage</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gong, Q</creatorcontrib><creatorcontrib>Xu, J.-F</creatorcontrib><creatorcontrib>Yin, H</creatorcontrib><creatorcontrib>Liu, S.-F</creatorcontrib><creatorcontrib>Duan, L.-H</creatorcontrib><creatorcontrib>Bian, Z.-L</creatorcontrib><collection>AGRIS</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>AIDS and Cancer Research Abstracts</collection><jtitle>Scandinavian journal of immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gong, Q</au><au>Xu, J.-F</au><au>Yin, H</au><au>Liu, S.-F</au><au>Duan, L.-H</au><au>Bian, Z.-L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective Effect of Antagonist of High-mobility Group Box 1 on Lipopolysaccharide-Induced Acute Lung Injury in Mice</atitle><jtitle>Scandinavian journal of immunology</jtitle><addtitle>Scand J Immunol</addtitle><date>2009</date><risdate>2009</risdate><volume>69</volume><issue>1</issue><spage>29</spage><epage>35</epage><pages>29-35</pages><issn>0300-9475</issn><eissn>1365-3083</eissn><abstract>We explored the effects of recombinant A-box (rA-box), a specific blockade for endogenous high mobility group box 1 (HMGB1) protein, on acute lung inflammation induced by lipopolysaccharide (LPS) in vivo. Acute lung injury (ALI) was produced successfully by intratracheal administration of LPS (10 μg/mouse) in male BALB/c mice. rA-box (0.3, 0.6 mg/mouse, i.p.) was administered 30 min prior to or 2 h after LPS exposure. Bronchoalveolar lavage fluid (BALF) was obtained to measure chemokines, proinflammatory cytokines, total cell counts and proteins at the indicated time points. It was found that rA-box caused a significant reduction in the total cells and neutrophils in BALF, a significant reduction in the W/D ratio and protein leakage at 24 h after LPS challenge. In addition, rA-box was also believed to have downregulated the expression of LPS-induced chemokines (keratinocyte-derived chemokine) and proinflammatory cytokines, including early mediator TNF-a and late mediator HMGB1. These findings confirm the significant protection of rA-box against LPS-induced ALI, and the effect mechanism of rA-box was associated with decreasing the expression of chemokines and proinflammatory cytokines.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>19140874</pmid><doi>10.1111/j.1365-3083.2008.02194.x</doi><tpages>7</tpages></addata></record> |
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| source | MEDLINE; Wiley Online Library Free Content; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library All Journals |
| subjects | Acute Lung Injury - chemically induced Acute Lung Injury - immunology Acute Lung Injury - prevention & control Amino Acid Motifs Animals Bronchoalveolar Lavage Fluid - immunology Chemokines - metabolism Down-Regulation - drug effects HMGB1 Protein - antagonists & inhibitors Inflammation Mediators - metabolism Injections, Intraperitoneal Lipopolysaccharides - immunology Male Mice Mice, Inbred BALB C Recombinant Proteins - administration & dosage Tumor Necrosis Factor-alpha - metabolism |
| title | Protective Effect of Antagonist of High-mobility Group Box 1 on Lipopolysaccharide-Induced Acute Lung Injury in Mice |
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