Urinary trypsin inhibitor reduces inflammatory response in kidney induced by Lipopolysaccharide
Human urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used in Japan as a drug for patients with acute inflammatory disorders such as septic shock and pancreatitis. Lipopolysaccharide (LPS) triggers the sepsis syndrome by activating monocytes to produce proinflammatory c...
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| Veröffentlicht in: | Journal of bioscience and bioengineering 2007-10, Vol.104 (4), p.315-320 |
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| creator | Ueki, Masaaki Taie, Satoshi Chujo, Kousuke Asaga, Takehiko Iwanaga, Yasuyuki Ono, Junichiro Maekawa, Nobuhiro |
| description | Human urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used in Japan as a drug for patients with acute inflammatory disorders such as septic shock and pancreatitis. Lipopolysaccharide (LPS) triggers the sepsis syndrome by activating monocytes to produce proinflammatory cytokines, including tumor necrosis factor alpha (TNFα), which potently stimulate the activation of neutrophils. The inhibitory mechanism of UTI on the systemic inflammatory response induced by the intraperitoneal injection of LPS in the kidney is unclear. This study was undertaken to examine the inhibitory effects of UTI on renal injury associated with the systemic inflammatory response induced by LPS stimulation, with emphasis on systemic TNFα and the activation of neutrophils in rat kidney. The systemic inflammatory response syndrome was induced by LPS treatment. Serum and renal TNFα, renal cytokine-induced neutrophil chemoattractant-1 (CINC-1) and myeloperoxidase (MPO) levels, as well as renal function after LPS stimulation, were evaluated. UTI (50,000 U/kg) inhibited LPS-induced increases in the serum and renal tissue levels of TNFα, as well as the renal tissue levels of CINC-1 and MPO after LPS stimulation. UTI (50,000 U/kg) also inhibited the production of serum TNFα associated with the systemic inflammatory response syndrome induced by LPS stimulation, thereby attenuating neutrophil infiltration into renal tissues and subsequent neutrophil-mediated renal injury. These findings may have important implications in understanding the biologic functions of UTI. UTI may prove useful in protecting against acute renal injury associated with a systemic inflammatory response. |
| doi_str_mv | 10.1263/jbb.104.315 |
| format | Article |
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Lipopolysaccharide (LPS) triggers the sepsis syndrome by activating monocytes to produce proinflammatory cytokines, including tumor necrosis factor alpha (TNFα), which potently stimulate the activation of neutrophils. The inhibitory mechanism of UTI on the systemic inflammatory response induced by the intraperitoneal injection of LPS in the kidney is unclear. This study was undertaken to examine the inhibitory effects of UTI on renal injury associated with the systemic inflammatory response induced by LPS stimulation, with emphasis on systemic TNFα and the activation of neutrophils in rat kidney. The systemic inflammatory response syndrome was induced by LPS treatment. Serum and renal TNFα, renal cytokine-induced neutrophil chemoattractant-1 (CINC-1) and myeloperoxidase (MPO) levels, as well as renal function after LPS stimulation, were evaluated. UTI (50,000 U/kg) inhibited LPS-induced increases in the serum and renal tissue levels of TNFα, as well as the renal tissue levels of CINC-1 and MPO after LPS stimulation. UTI (50,000 U/kg) also inhibited the production of serum TNFα associated with the systemic inflammatory response syndrome induced by LPS stimulation, thereby attenuating neutrophil infiltration into renal tissues and subsequent neutrophil-mediated renal injury. These findings may have important implications in understanding the biologic functions of UTI. UTI may prove useful in protecting against acute renal injury associated with a systemic inflammatory response.</description><identifier>ISSN: 1389-1723</identifier><identifier>EISSN: 1347-4421</identifier><identifier>DOI: 10.1263/jbb.104.315</identifier><identifier>PMID: 18023806</identifier><identifier>CODEN: JFBIEX</identifier><language>eng</language><publisher>Amsterdarm: Elsevier B.V</publisher><subject>acute renal dysfunction ; Animals ; Anti-Inflammatory Agents - administration & dosage ; Biological and medical sciences ; Biotechnology ; cytokine-induced neutrophil chemoattractant-1 (CINC-1) ; Cytokines - immunology ; Dose-Response Relationship, Drug ; Fundamental and applied biological sciences. Psychology ; Glycoproteins - administration & dosage ; INFLAMACION ; INFLAMMATION ; INHIBIDORES DE TRIPSINA ; INHIBITEUR DE TRYPSINE ; Kidney - drug effects ; Kidney - immunology ; KIDNEYS ; LIPOPOLISACARIDOS ; LIPOPOLYSACCHARIDE ; LIPOPOLYSACCHARIDES ; Male ; Nephritis - chemically induced ; Nephritis - immunology ; Nephritis - prevention & control ; neutrophil ; ORINA ; Rats ; Rats, Wistar ; REIN ; RINONES ; TRYPSIN INHIBITORS ; tumor necrosis factor alpha ; urinary trypsin inhibitor ; URINE</subject><ispartof>Journal of bioscience and bioengineering, 2007-10, Vol.104 (4), p.315-320</ispartof><rights>2007 The Society for Biotechnology, Japan</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Japan Science and Technology Agency 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-d4bcbb182d9cb767523266b235b8f8fe99e56d77a007d10e52900e10d46c22dd3</citedby><cites>FETCH-LOGICAL-c559t-d4bcbb182d9cb767523266b235b8f8fe99e56d77a007d10e52900e10d46c22dd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1389172307701652$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19228644$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18023806$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ueki, Masaaki</creatorcontrib><creatorcontrib>Taie, Satoshi</creatorcontrib><creatorcontrib>Chujo, Kousuke</creatorcontrib><creatorcontrib>Asaga, Takehiko</creatorcontrib><creatorcontrib>Iwanaga, Yasuyuki</creatorcontrib><creatorcontrib>Ono, Junichiro</creatorcontrib><creatorcontrib>Maekawa, Nobuhiro</creatorcontrib><title>Urinary trypsin inhibitor reduces inflammatory response in kidney induced by Lipopolysaccharide</title><title>Journal of bioscience and bioengineering</title><addtitle>J Biosci Bioeng</addtitle><description>Human urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used in Japan as a drug for patients with acute inflammatory disorders such as septic shock and pancreatitis. Lipopolysaccharide (LPS) triggers the sepsis syndrome by activating monocytes to produce proinflammatory cytokines, including tumor necrosis factor alpha (TNFα), which potently stimulate the activation of neutrophils. The inhibitory mechanism of UTI on the systemic inflammatory response induced by the intraperitoneal injection of LPS in the kidney is unclear. This study was undertaken to examine the inhibitory effects of UTI on renal injury associated with the systemic inflammatory response induced by LPS stimulation, with emphasis on systemic TNFα and the activation of neutrophils in rat kidney. The systemic inflammatory response syndrome was induced by LPS treatment. Serum and renal TNFα, renal cytokine-induced neutrophil chemoattractant-1 (CINC-1) and myeloperoxidase (MPO) levels, as well as renal function after LPS stimulation, were evaluated. UTI (50,000 U/kg) inhibited LPS-induced increases in the serum and renal tissue levels of TNFα, as well as the renal tissue levels of CINC-1 and MPO after LPS stimulation. UTI (50,000 U/kg) also inhibited the production of serum TNFα associated with the systemic inflammatory response syndrome induced by LPS stimulation, thereby attenuating neutrophil infiltration into renal tissues and subsequent neutrophil-mediated renal injury. These findings may have important implications in understanding the biologic functions of UTI. UTI may prove useful in protecting against acute renal injury associated with a systemic inflammatory response.</description><subject>acute renal dysfunction</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - administration & dosage</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>cytokine-induced neutrophil chemoattractant-1 (CINC-1)</subject><subject>Cytokines - immunology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glycoproteins - administration & dosage</subject><subject>INFLAMACION</subject><subject>INFLAMMATION</subject><subject>INHIBIDORES DE TRIPSINA</subject><subject>INHIBITEUR DE TRYPSINE</subject><subject>Kidney - drug effects</subject><subject>Kidney - immunology</subject><subject>KIDNEYS</subject><subject>LIPOPOLISACARIDOS</subject><subject>LIPOPOLYSACCHARIDE</subject><subject>LIPOPOLYSACCHARIDES</subject><subject>Male</subject><subject>Nephritis - chemically induced</subject><subject>Nephritis - immunology</subject><subject>Nephritis - prevention & control</subject><subject>neutrophil</subject><subject>ORINA</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>REIN</subject><subject>RINONES</subject><subject>TRYPSIN INHIBITORS</subject><subject>tumor necrosis factor alpha</subject><subject>urinary trypsin inhibitor</subject><subject>URINE</subject><issn>1389-1723</issn><issn>1347-4421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkUuL1EAURoMozkNXrpWAjBtJW89UaimDTxp04ayLetw41SapWJUI-ffephsGxFV9fPdwuZyqqheU7Chr-buDcztKxI5T-ai6pFyoRghGHx9zpxuqGL-orko5EEIVUfRpdUE7wnhH2svK3OU42bzVS97mEqc6TvfRxSXlOkNYPRRs-sGOo8Vuw7LMaSqAbf0rhgk2TEcu1G6r93FOcxq2Yr2_tzkGeFY96e1Q4Pn5va7uPn74cfu52X_79OX2_b7xUuqlCcJ552jHgvZOtUoyztrWMS5d13c9aA2yDUpZQlSgBCTThAAlQbSesRD4dfXmtHfO6fcKZTFjLB6GwU6Q1mIYkaoVTCL4-h_wkNY84W2GCkE505oppN6eKJ9TKRl6M-c4oidDiTlaN2gdszBoHelX552rGyE8sGfNCNycAVu8HfpsJx_LA6cZ61ohkHt54nqbjP2Zkfn6nRHS4ddJonEuT3NAlX8iZFN8hAntxwx-MSHF_x74F5Khpac</recordid><startdate>20071001</startdate><enddate>20071001</enddate><creator>Ueki, Masaaki</creator><creator>Taie, Satoshi</creator><creator>Chujo, Kousuke</creator><creator>Asaga, Takehiko</creator><creator>Iwanaga, Yasuyuki</creator><creator>Ono, Junichiro</creator><creator>Maekawa, Nobuhiro</creator><general>Elsevier B.V</general><general>Elsevier Science</general><general>Elsevier Limited</general><scope>FBQ</scope><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>7QL</scope><scope>7QO</scope><scope>7T5</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>20071001</creationdate><title>Urinary trypsin inhibitor reduces inflammatory response in kidney induced by Lipopolysaccharide</title><author>Ueki, Masaaki ; Taie, Satoshi ; Chujo, Kousuke ; Asaga, Takehiko ; Iwanaga, Yasuyuki ; Ono, Junichiro ; Maekawa, Nobuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-d4bcbb182d9cb767523266b235b8f8fe99e56d77a007d10e52900e10d46c22dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>acute renal dysfunction</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - administration & dosage</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>cytokine-induced neutrophil chemoattractant-1 (CINC-1)</topic><topic>Cytokines - immunology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glycoproteins - administration & dosage</topic><topic>INFLAMACION</topic><topic>INFLAMMATION</topic><topic>INHIBIDORES DE TRIPSINA</topic><topic>INHIBITEUR DE TRYPSINE</topic><topic>Kidney - drug effects</topic><topic>Kidney - immunology</topic><topic>KIDNEYS</topic><topic>LIPOPOLISACARIDOS</topic><topic>LIPOPOLYSACCHARIDE</topic><topic>LIPOPOLYSACCHARIDES</topic><topic>Male</topic><topic>Nephritis - chemically induced</topic><topic>Nephritis - immunology</topic><topic>Nephritis - prevention & control</topic><topic>neutrophil</topic><topic>ORINA</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>REIN</topic><topic>RINONES</topic><topic>TRYPSIN INHIBITORS</topic><topic>tumor necrosis factor alpha</topic><topic>urinary trypsin inhibitor</topic><topic>URINE</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ueki, Masaaki</creatorcontrib><creatorcontrib>Taie, Satoshi</creatorcontrib><creatorcontrib>Chujo, Kousuke</creatorcontrib><creatorcontrib>Asaga, Takehiko</creatorcontrib><creatorcontrib>Iwanaga, Yasuyuki</creatorcontrib><creatorcontrib>Ono, Junichiro</creatorcontrib><creatorcontrib>Maekawa, Nobuhiro</creatorcontrib><collection>AGRIS</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of bioscience and bioengineering</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ueki, Masaaki</au><au>Taie, Satoshi</au><au>Chujo, Kousuke</au><au>Asaga, Takehiko</au><au>Iwanaga, Yasuyuki</au><au>Ono, Junichiro</au><au>Maekawa, Nobuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Urinary trypsin inhibitor reduces inflammatory response in kidney induced by Lipopolysaccharide</atitle><jtitle>Journal of bioscience and bioengineering</jtitle><addtitle>J Biosci Bioeng</addtitle><date>2007-10-01</date><risdate>2007</risdate><volume>104</volume><issue>4</issue><spage>315</spage><epage>320</epage><pages>315-320</pages><issn>1389-1723</issn><eissn>1347-4421</eissn><coden>JFBIEX</coden><abstract>Human urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used in Japan as a drug for patients with acute inflammatory disorders such as septic shock and pancreatitis. Lipopolysaccharide (LPS) triggers the sepsis syndrome by activating monocytes to produce proinflammatory cytokines, including tumor necrosis factor alpha (TNFα), which potently stimulate the activation of neutrophils. The inhibitory mechanism of UTI on the systemic inflammatory response induced by the intraperitoneal injection of LPS in the kidney is unclear. This study was undertaken to examine the inhibitory effects of UTI on renal injury associated with the systemic inflammatory response induced by LPS stimulation, with emphasis on systemic TNFα and the activation of neutrophils in rat kidney. The systemic inflammatory response syndrome was induced by LPS treatment. Serum and renal TNFα, renal cytokine-induced neutrophil chemoattractant-1 (CINC-1) and myeloperoxidase (MPO) levels, as well as renal function after LPS stimulation, were evaluated. UTI (50,000 U/kg) inhibited LPS-induced increases in the serum and renal tissue levels of TNFα, as well as the renal tissue levels of CINC-1 and MPO after LPS stimulation. UTI (50,000 U/kg) also inhibited the production of serum TNFα associated with the systemic inflammatory response syndrome induced by LPS stimulation, thereby attenuating neutrophil infiltration into renal tissues and subsequent neutrophil-mediated renal injury. These findings may have important implications in understanding the biologic functions of UTI. UTI may prove useful in protecting against acute renal injury associated with a systemic inflammatory response.</abstract><cop>Amsterdarm</cop><pub>Elsevier B.V</pub><pmid>18023806</pmid><doi>10.1263/jbb.104.315</doi><tpages>6</tpages></addata></record> |
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| subjects | acute renal dysfunction Animals Anti-Inflammatory Agents - administration & dosage Biological and medical sciences Biotechnology cytokine-induced neutrophil chemoattractant-1 (CINC-1) Cytokines - immunology Dose-Response Relationship, Drug Fundamental and applied biological sciences. Psychology Glycoproteins - administration & dosage INFLAMACION INFLAMMATION INHIBIDORES DE TRIPSINA INHIBITEUR DE TRYPSINE Kidney - drug effects Kidney - immunology KIDNEYS LIPOPOLISACARIDOS LIPOPOLYSACCHARIDE LIPOPOLYSACCHARIDES Male Nephritis - chemically induced Nephritis - immunology Nephritis - prevention & control neutrophil ORINA Rats Rats, Wistar REIN RINONES TRYPSIN INHIBITORS tumor necrosis factor alpha urinary trypsin inhibitor URINE |
| title | Urinary trypsin inhibitor reduces inflammatory response in kidney induced by Lipopolysaccharide |
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