Caspase-1-processed interleukins in hyperoxia-induced cell death in the developing brain
Infants born prematurely may develop neurocognitive deficits without an obvious cause. Oxygen, which is widely used in neonatal medicine, constitutes one possible contributing neurotoxic factor, because it can trigger neuronal apoptosis in the developing brain of rodents. We hypothesized that two ca...
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| Veröffentlicht in: | Annals of neurology 2005-01, Vol.57 (1), p.50-59 |
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| creator | Felderhoff-Mueser, Ursula Sifringer, Marco Polley, Oliver Dzietko, Mark Leineweber, Birgit Mahler, Lieselotte Baier, Michael Bittigau, Petra Obladen, Michael Ikonomidou, Chrysanthy Bührer, Christoph |
| description | Infants born prematurely may develop neurocognitive deficits without an obvious cause. Oxygen, which is widely used in neonatal medicine, constitutes one possible contributing neurotoxic factor, because it can trigger neuronal apoptosis in the developing brain of rodents. We hypothesized that two caspase‐1–processed cytokines, interleukin (IL)–1β and IL‐18, are involved in oxygen‐induced neuronal cell death. Six‐day‐old Wistar rats or C57/BL6 mice were exposed to 80% oxygen for various time periods (2, 6, 12, 24, and 48 hours). Neuronal cell death in the brain, as assessed by Fluoro‐Jade B and silver staining, peaked at 12 to 24 hours and was preceded by a marked increase in mRNA and protein levels of caspase 1, IL‐1β, IL‐18, and IL‐18 receptor α (IL‐18Rα). Intraperitoneal injection of recombinant human IL‐18–binding protein, a specific inhibitor of IL‐18, attenuated hyperoxic brain injury. Mice deficient in IL‐1 receptor–associated kinase 4 (IRAK‐4), which is pivotal for both IL‐1β and IL‐18 signal transduction, were protected against oxygen‐mediated neurotoxicity. These findings causally link IL‐1β and IL‐18 to hyperoxia‐induced cell death in the immature brain. These cytokines might serve as useful targets for therapeutic approaches aimed at preserving neuronal function in the immature brain, which is exquisitely sensitive to a variety of iatrogenic measures including oxygen. Ann Neurol 2005;57:50–59 |
| doi_str_mv | 10.1002/ana.20322 |
| format | Article |
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Oxygen, which is widely used in neonatal medicine, constitutes one possible contributing neurotoxic factor, because it can trigger neuronal apoptosis in the developing brain of rodents. We hypothesized that two caspase‐1–processed cytokines, interleukin (IL)–1β and IL‐18, are involved in oxygen‐induced neuronal cell death. Six‐day‐old Wistar rats or C57/BL6 mice were exposed to 80% oxygen for various time periods (2, 6, 12, 24, and 48 hours). Neuronal cell death in the brain, as assessed by Fluoro‐Jade B and silver staining, peaked at 12 to 24 hours and was preceded by a marked increase in mRNA and protein levels of caspase 1, IL‐1β, IL‐18, and IL‐18 receptor α (IL‐18Rα). Intraperitoneal injection of recombinant human IL‐18–binding protein, a specific inhibitor of IL‐18, attenuated hyperoxic brain injury. Mice deficient in IL‐1 receptor–associated kinase 4 (IRAK‐4), which is pivotal for both IL‐1β and IL‐18 signal transduction, were protected against oxygen‐mediated neurotoxicity. These findings causally link IL‐1β and IL‐18 to hyperoxia‐induced cell death in the immature brain. These cytokines might serve as useful targets for therapeutic approaches aimed at preserving neuronal function in the immature brain, which is exquisitely sensitive to a variety of iatrogenic measures including oxygen. Ann Neurol 2005;57:50–59</description><identifier>ISSN: 0364-5134</identifier><identifier>EISSN: 1531-8249</identifier><identifier>DOI: 10.1002/ana.20322</identifier><identifier>PMID: 15622543</identifier><identifier>CODEN: ANNED3</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Animals, Newborn ; Biological and medical sciences ; Blotting, Western - methods ; Brain - drug effects ; Brain - growth & development ; Brain - pathology ; Caspase 1 - genetics ; Caspase 1 - metabolism ; Cell Death - physiology ; Development. Senescence. Regeneration. Transplantation ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug toxicity and drugs side effects treatment ; Fundamental and applied biological sciences. Psychology ; Hyperoxia - pathology ; Immunohistochemistry - methods ; In Situ Nick-End Labeling - methods ; Interleukin-1 - pharmacology ; Interleukin-1 Receptor-Associated Kinases ; Interleukin-18 - pharmacology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Degeneration - genetics ; Nerve Degeneration - metabolism ; Neurology ; Oxygen - toxicity ; Pharmacology. Drug treatments ; Phosphotransferases (Alcohol Group Acceptor) - deficiency ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - metabolism ; Time Factors ; Toxicity: nervous system and muscle ; Vertebrates: nervous system and sense organs</subject><ispartof>Annals of neurology, 2005-01, Vol.57 (1), p.50-59</ispartof><rights>Copyright © 2004 American Neurological Association</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5232-6f9df1c8fc688a60d4f7bb5afead570b71b716426fd23e05c2b29b8d0409507c3</citedby><cites>FETCH-LOGICAL-c5232-6f9df1c8fc688a60d4f7bb5afead570b71b716426fd23e05c2b29b8d0409507c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fana.20322$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fana.20322$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16570585$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15622543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Felderhoff-Mueser, Ursula</creatorcontrib><creatorcontrib>Sifringer, Marco</creatorcontrib><creatorcontrib>Polley, Oliver</creatorcontrib><creatorcontrib>Dzietko, Mark</creatorcontrib><creatorcontrib>Leineweber, Birgit</creatorcontrib><creatorcontrib>Mahler, Lieselotte</creatorcontrib><creatorcontrib>Baier, Michael</creatorcontrib><creatorcontrib>Bittigau, Petra</creatorcontrib><creatorcontrib>Obladen, Michael</creatorcontrib><creatorcontrib>Ikonomidou, Chrysanthy</creatorcontrib><creatorcontrib>Bührer, Christoph</creatorcontrib><title>Caspase-1-processed interleukins in hyperoxia-induced cell death in the developing brain</title><title>Annals of neurology</title><addtitle>Ann Neurol</addtitle><description>Infants born prematurely may develop neurocognitive deficits without an obvious cause. Oxygen, which is widely used in neonatal medicine, constitutes one possible contributing neurotoxic factor, because it can trigger neuronal apoptosis in the developing brain of rodents. We hypothesized that two caspase‐1–processed cytokines, interleukin (IL)–1β and IL‐18, are involved in oxygen‐induced neuronal cell death. Six‐day‐old Wistar rats or C57/BL6 mice were exposed to 80% oxygen for various time periods (2, 6, 12, 24, and 48 hours). Neuronal cell death in the brain, as assessed by Fluoro‐Jade B and silver staining, peaked at 12 to 24 hours and was preceded by a marked increase in mRNA and protein levels of caspase 1, IL‐1β, IL‐18, and IL‐18 receptor α (IL‐18Rα). Intraperitoneal injection of recombinant human IL‐18–binding protein, a specific inhibitor of IL‐18, attenuated hyperoxic brain injury. Mice deficient in IL‐1 receptor–associated kinase 4 (IRAK‐4), which is pivotal for both IL‐1β and IL‐18 signal transduction, were protected against oxygen‐mediated neurotoxicity. These findings causally link IL‐1β and IL‐18 to hyperoxia‐induced cell death in the immature brain. These cytokines might serve as useful targets for therapeutic approaches aimed at preserving neuronal function in the immature brain, which is exquisitely sensitive to a variety of iatrogenic measures including oxygen. Ann Neurol 2005;57:50–59</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western - methods</subject><subject>Brain - drug effects</subject><subject>Brain - growth & development</subject><subject>Brain - pathology</subject><subject>Caspase 1 - genetics</subject><subject>Caspase 1 - metabolism</subject><subject>Cell Death - physiology</subject><subject>Development. Senescence. Regeneration. Transplantation</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug toxicity and drugs side effects treatment</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hyperoxia - pathology</subject><subject>Immunohistochemistry - methods</subject><subject>In Situ Nick-End Labeling - methods</subject><subject>Interleukin-1 - pharmacology</subject><subject>Interleukin-1 Receptor-Associated Kinases</subject><subject>Interleukin-18 - pharmacology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nerve Degeneration - genetics</subject><subject>Nerve Degeneration - metabolism</subject><subject>Neurology</subject><subject>Oxygen - toxicity</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - deficiency</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - metabolism</subject><subject>Time Factors</subject><subject>Toxicity: nervous system and muscle</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0364-5134</issn><issn>1531-8249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFv1DAQha0K1C6lh_4BtJcicXA7tmMnOS4rWpCqghCIqhfLsces22wS7AS6_x4vu9AT0kij0Xwz7-kRcsrgnAHwC9OZcw6C8wMyY1IwWvGifkZmIFRBJRPFEXmR0j0A1IrBITliUnEuCzEjt0uTBpOQMjrE3mJK6OahGzG2OD2ELuVhvtoMGPvHYGjo3GQzYbFt5w7NuNruxxXm4Se2_RC67_MmmtC9JM-9aROe7Psx-Xr57svyPb3-ePVhubimVnLBqfK188xW3qqqMgpc4cumkcajcbKEpmS5VMGVd1wgSMsbXjeVgwJqCaUVx-T17m-2_2PCNOp1SFt7psN-SpqVAnglVQbf7EAb-5Qiej3EsDZxoxnobYw6x6j_xJjZV_unU7NG90Tuc8vA2R4wyZrWR9PZkJ44lb3LSmbuYsf9Ci1u_q-oFzeLv9J0dxHSiI__Lkx80KoUpdTfbq60-szY3ae3l5qL3xCWmBA</recordid><startdate>200501</startdate><enddate>200501</enddate><creator>Felderhoff-Mueser, Ursula</creator><creator>Sifringer, Marco</creator><creator>Polley, Oliver</creator><creator>Dzietko, Mark</creator><creator>Leineweber, Birgit</creator><creator>Mahler, Lieselotte</creator><creator>Baier, Michael</creator><creator>Bittigau, Petra</creator><creator>Obladen, Michael</creator><creator>Ikonomidou, Chrysanthy</creator><creator>Bührer, Christoph</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Willey-Liss</general><scope>BSCLL</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>7TK</scope></search><sort><creationdate>200501</creationdate><title>Caspase-1-processed interleukins in hyperoxia-induced cell death in the developing brain</title><author>Felderhoff-Mueser, Ursula ; Sifringer, Marco ; Polley, Oliver ; Dzietko, Mark ; Leineweber, Birgit ; Mahler, Lieselotte ; Baier, Michael ; Bittigau, Petra ; Obladen, Michael ; Ikonomidou, Chrysanthy ; Bührer, Christoph</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5232-6f9df1c8fc688a60d4f7bb5afead570b71b716426fd23e05c2b29b8d0409507c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western - methods</topic><topic>Brain - drug effects</topic><topic>Brain - growth & development</topic><topic>Brain - pathology</topic><topic>Caspase 1 - genetics</topic><topic>Caspase 1 - metabolism</topic><topic>Cell Death - physiology</topic><topic>Development. Senescence. Regeneration. Transplantation</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug toxicity and drugs side effects treatment</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hyperoxia - pathology</topic><topic>Immunohistochemistry - methods</topic><topic>In Situ Nick-End Labeling - methods</topic><topic>Interleukin-1 - pharmacology</topic><topic>Interleukin-1 Receptor-Associated Kinases</topic><topic>Interleukin-18 - pharmacology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Nerve Degeneration - genetics</topic><topic>Nerve Degeneration - metabolism</topic><topic>Neurology</topic><topic>Oxygen - toxicity</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - deficiency</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - metabolism</topic><topic>Time Factors</topic><topic>Toxicity: nervous system and muscle</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Felderhoff-Mueser, Ursula</creatorcontrib><creatorcontrib>Sifringer, Marco</creatorcontrib><creatorcontrib>Polley, Oliver</creatorcontrib><creatorcontrib>Dzietko, Mark</creatorcontrib><creatorcontrib>Leineweber, Birgit</creatorcontrib><creatorcontrib>Mahler, Lieselotte</creatorcontrib><creatorcontrib>Baier, Michael</creatorcontrib><creatorcontrib>Bittigau, Petra</creatorcontrib><creatorcontrib>Obladen, Michael</creatorcontrib><creatorcontrib>Ikonomidou, Chrysanthy</creatorcontrib><creatorcontrib>Bührer, Christoph</creatorcontrib><collection>Istex</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>Neurosciences Abstracts</collection><jtitle>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Felderhoff-Mueser, Ursula</au><au>Sifringer, Marco</au><au>Polley, Oliver</au><au>Dzietko, Mark</au><au>Leineweber, Birgit</au><au>Mahler, Lieselotte</au><au>Baier, Michael</au><au>Bittigau, Petra</au><au>Obladen, Michael</au><au>Ikonomidou, Chrysanthy</au><au>Bührer, Christoph</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Caspase-1-processed interleukins in hyperoxia-induced cell death in the developing brain</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>2005-01</date><risdate>2005</risdate><volume>57</volume><issue>1</issue><spage>50</spage><epage>59</epage><pages>50-59</pages><issn>0364-5134</issn><eissn>1531-8249</eissn><coden>ANNED3</coden><abstract>Infants born prematurely may develop neurocognitive deficits without an obvious cause. Oxygen, which is widely used in neonatal medicine, constitutes one possible contributing neurotoxic factor, because it can trigger neuronal apoptosis in the developing brain of rodents. We hypothesized that two caspase‐1–processed cytokines, interleukin (IL)–1β and IL‐18, are involved in oxygen‐induced neuronal cell death. Six‐day‐old Wistar rats or C57/BL6 mice were exposed to 80% oxygen for various time periods (2, 6, 12, 24, and 48 hours). Neuronal cell death in the brain, as assessed by Fluoro‐Jade B and silver staining, peaked at 12 to 24 hours and was preceded by a marked increase in mRNA and protein levels of caspase 1, IL‐1β, IL‐18, and IL‐18 receptor α (IL‐18Rα). Intraperitoneal injection of recombinant human IL‐18–binding protein, a specific inhibitor of IL‐18, attenuated hyperoxic brain injury. Mice deficient in IL‐1 receptor–associated kinase 4 (IRAK‐4), which is pivotal for both IL‐1β and IL‐18 signal transduction, were protected against oxygen‐mediated neurotoxicity. These findings causally link IL‐1β and IL‐18 to hyperoxia‐induced cell death in the immature brain. These cytokines might serve as useful targets for therapeutic approaches aimed at preserving neuronal function in the immature brain, which is exquisitely sensitive to a variety of iatrogenic measures including oxygen. Ann Neurol 2005;57:50–59</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>15622543</pmid><doi>10.1002/ana.20322</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Animals, Newborn Biological and medical sciences Blotting, Western - methods Brain - drug effects Brain - growth & development Brain - pathology Caspase 1 - genetics Caspase 1 - metabolism Cell Death - physiology Development. Senescence. Regeneration. Transplantation Disease Models, Animal Dose-Response Relationship, Drug Drug toxicity and drugs side effects treatment Fundamental and applied biological sciences. Psychology Hyperoxia - pathology Immunohistochemistry - methods In Situ Nick-End Labeling - methods Interleukin-1 - pharmacology Interleukin-1 Receptor-Associated Kinases Interleukin-18 - pharmacology Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Nerve Degeneration - genetics Nerve Degeneration - metabolism Neurology Oxygen - toxicity Pharmacology. Drug treatments Phosphotransferases (Alcohol Group Acceptor) - deficiency Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - metabolism Time Factors Toxicity: nervous system and muscle Vertebrates: nervous system and sense organs |
| title | Caspase-1-processed interleukins in hyperoxia-induced cell death in the developing brain |
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