Nitric oxide synthase isoforms play distinct roles during acute peritonitis
Identifieur interne : 001470 ( Istex/Curation ); précédent : 001469; suivant : 001471Nitric oxide synthase isoforms play distinct roles during acute peritonitis
Auteurs : Jie Ni [Belgique] ; Rachel M. Mcloughlin [Royaume-Uni] ; Alexandre Brodovitch [Belgique] ; Pierre Moulin [Belgique] ; Peter Brouckaert [Belgique] ; Barbara Casadei [Royaume-Uni] ; Olivier Feron [Belgique] ; Nicholas Topley [Royaume-Uni] ; Jean-Luc. Balligand [Belgique] ; Olivier Devuyst [Belgique]Source :
- Nephrology Dialysis Transplantation [ 0931-0509 ] ; 2010-01.
Abstract
Background. Acute peritonitis is the most frequent complication of peritoneal dialysis (PD). Increased nitric oxide (NO) release by NO synthase (NOS) isoforms has been implicated in acute peritonitis, but the role played by the NOS isoforms expressed in the peritoneum is unknown. Methods. We investigated the structural and functional consequences of acute peritonitis induced by LPS in wild-type (WT) mice versus knockout mice (KO) for the endothelial NOS (eNOS), the inducible NOS (iNOS) or the neuronal NOS (nNOS). Results. The level of NO metabolites (NOx) in the dialysate was maximal 18 h after LPS injection. LPS induced a significant increase in the transport of small solutes and decreased ultrafiltration in WT mice. These changes, which occurred without vascular proliferation, were paralleled by the upregulation of nNOS and eNOS, and the induction of iNOS. The transport modifications induced by LPS were significantly reversed in eNOS KO mice, but not modified in mice lacking iNOS or nNOS. In contrast, the increase of dialysate NOx was abolished in iNOS KO mice and significantly reduced in eNOS KO mice, but left unchanged in mice lacking nNOS. Mice lacking iNOS also showed more severe inflammatory changes, and a trend towards increased mortality following LPS. Conclusion. These data demonstrate specific roles for NOS isoforms in the peritoneal membrane and suggest that selective eNOS inhibition may improve peritoneal transport during acute peritonitis.
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DOI: 10.1093/ndt/gfp415
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Balligand</name><affiliation wicri:level="1"><mods:affiliation>Universit catholique de Louvain Medical School, Brussels, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Universit catholique de Louvain Medical School, Brussels</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation><wicri:noCountry code="no comma">Correspondence and offprint requests to: Olivier Devuyst;</wicri:noCountry></affiliation></author><author><name sortKey="Devuyst, Olivier" sort="Devuyst, Olivier" uniqKey="Devuyst O" first="Olivier" last="Devuyst">Olivier Devuyst</name><affiliation wicri:level="1"><mods:affiliation>Universit catholique de Louvain Medical School, Brussels, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Universit catholique de Louvain Medical School, Brussels</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation><wicri:noCountry code="no comma">Correspondence and offprint requests to: Olivier Devuyst;</wicri:noCountry></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:4CFEE118C4368BAD913AB5ADF601AA7C1F4054D5</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1093/ndt/gfp415</idno><idno type="url">https://api.istex.fr/document/4CFEE118C4368BAD913AB5ADF601AA7C1F4054D5/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001517</idno><idno type="wicri:Area/Istex/Curation">001470</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Nitric oxide synthase isoforms play distinct roles during acute peritonitis</title><author><name sortKey="Ni, Jie" sort="Ni, Jie" uniqKey="Ni J" first="Jie" last="Ni">Jie Ni</name><affiliation wicri:level="1"><mods:affiliation>Universit catholique de Louvain Medical School, Brussels, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Universit catholique de Louvain Medical School, Brussels</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Mcloughlin, Rachel M" sort="Mcloughlin, Rachel M" uniqKey="Mcloughlin R" first="Rachel M." last="Mcloughlin">Rachel M. Mcloughlin</name><affiliation wicri:level="1"><mods:affiliation>School of Medicine, Cardiff University, Cardiff, UK</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>School of Medicine, Cardiff University, Cardiff</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Brodovitch, Alexandre" sort="Brodovitch, Alexandre" uniqKey="Brodovitch A" first="Alexandre" last="Brodovitch">Alexandre Brodovitch</name><affiliation wicri:level="1"><mods:affiliation>Universit catholique de Louvain Medical School, Brussels, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Universit catholique de Louvain Medical School, Brussels</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Moulin, Pierre" sort="Moulin, Pierre" uniqKey="Moulin P" first="Pierre" last="Moulin">Pierre Moulin</name><affiliation wicri:level="1"><mods:affiliation>Universit catholique de Louvain Medical School, Brussels, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Universit catholique de Louvain Medical School, Brussels</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Brouckaert, Peter" sort="Brouckaert, Peter" uniqKey="Brouckaert P" first="Peter" last="Brouckaert">Peter Brouckaert</name><affiliation wicri:level="1"><mods:affiliation>Department for Molecular Biomedical Research, VIB and Department for Biomedical Molecular Biology, Ghent University, Ghent, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Department for Molecular Biomedical Research, VIB and Department for Biomedical Molecular Biology, Ghent University, Ghent</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Casadei, Barbara" sort="Casadei, Barbara" uniqKey="Casadei B" first="Barbara" last="Casadei">Barbara Casadei</name><affiliation wicri:level="1"><mods:affiliation>University Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, UK</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>University Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Feron, Olivier" sort="Feron, Olivier" uniqKey="Feron O" first="Olivier" last="Feron">Olivier Feron</name><affiliation wicri:level="1"><mods:affiliation>Universit catholique de Louvain Medical School, Brussels, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Universit catholique de Louvain Medical School, Brussels</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Topley, Nicholas" sort="Topley, Nicholas" uniqKey="Topley N" first="Nicholas" last="Topley">Nicholas Topley</name><affiliation wicri:level="1"><mods:affiliation>School of Medicine, Cardiff University, Cardiff, UK</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>School of Medicine, Cardiff University, Cardiff</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Balligand, Jean Luc" sort="Balligand, Jean Luc" uniqKey="Balligand J" first="Jean-Luc." last="Balligand">Jean-Luc. Balligand</name><affiliation wicri:level="1"><mods:affiliation>Universit catholique de Louvain Medical School, Brussels, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Universit catholique de Louvain Medical School, Brussels</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author><author><name sortKey="Devuyst, Olivier" sort="Devuyst, Olivier" uniqKey="Devuyst O" first="Olivier" last="Devuyst">Olivier Devuyst</name><affiliation wicri:level="1"><mods:affiliation>Universit catholique de Louvain Medical School, Brussels, Belgium</mods:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Universit catholique de Louvain Medical School, Brussels</wicri:regionArea></affiliation><affiliation><mods:affiliation>Correspondence and offprint requests to: Olivier Devuyst;</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Nephrology Dialysis Transplantation</title><title level="j" type="abbrev">Nephrol Dial Transplant</title><idno type="ISSN">0931-0509</idno><idno type="eISSN">1460-2385</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2010-01">2010-01</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="86">86</biblScope><biblScope unit="page" to="96">96</biblScope></imprint><idno type="ISSN">0931-0509</idno></series><idno type="istex">4CFEE118C4368BAD913AB5ADF601AA7C1F4054D5</idno><idno type="DOI">10.1093/ndt/gfp415</idno><idno type="ArticleID">gfp415</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0931-0509</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background. Acute peritonitis is the most frequent complication of peritoneal dialysis (PD). Increased nitric oxide (NO) release by NO synthase (NOS) isoforms has been implicated in acute peritonitis, but the role played by the NOS isoforms expressed in the peritoneum is unknown. Methods. We investigated the structural and functional consequences of acute peritonitis induced by LPS in wild-type (WT) mice versus knockout mice (KO) for the endothelial NOS (eNOS), the inducible NOS (iNOS) or the neuronal NOS (nNOS). Results. The level of NO metabolites (NOx) in the dialysate was maximal 18 h after LPS injection. LPS induced a significant increase in the transport of small solutes and decreased ultrafiltration in WT mice. These changes, which occurred without vascular proliferation, were paralleled by the upregulation of nNOS and eNOS, and the induction of iNOS. The transport modifications induced by LPS were significantly reversed in eNOS KO mice, but not modified in mice lacking iNOS or nNOS. In contrast, the increase of dialysate NOx was abolished in iNOS KO mice and significantly reduced in eNOS KO mice, but left unchanged in mice lacking nNOS. Mice lacking iNOS also showed more severe inflammatory changes, and a trend towards increased mortality following LPS. Conclusion. These data demonstrate specific roles for NOS isoforms in the peritoneal membrane and suggest that selective eNOS inhibition may improve peritoneal transport during acute peritonitis.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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