Local interaction of apoptotic hepatocytes and Kupffer cells in a rat model of systemic endotoxemia
Identifieur interne : 000850 ( Main/Exploration ); précédent : 000849; suivant : 000851Local interaction of apoptotic hepatocytes and Kupffer cells in a rat model of systemic endotoxemia
Auteurs : Christian Eipel [Allemagne] ; Martin Hirschmann ; Kerstin Abshagen ; Michael D. Menger [Allemagne] ; Brigitte VollmarSource :
- Hepatology Research [ 1386-6346 ] ; 2007-10.
English descriptors
- KwdEn :
- Teeft :
- Adherent, Adherent latex particles, Apoptosis, Apoptotic, Apoptotic bodies, Apoptotic cell death, Apoptotic hepatocytes, Coli, Colocalization, Control animals, Direct vicinity, Eipel, Endotoxemic, Endotoxemic animals, Equivalent volume, Experimental surgery, Gadolinium chloride, Hepatic, Hepatocellular, Hepatocellular apoptosis, Hepatocyte apoptosis, Hepatocytes, Hepatology, Hepatology hepatology research, Hepatology research, Intraperitoneal, Intravital, Isotonic saline, Japan society, Kupffer, Kupffer cells, Latex, Latex particles, Leukocyte, Liver injury, Liver tissue, Macrophage, Menger, Observation period, Parenchymal, Physiol, Platelet, Postsinusoidal venules, Quantitative analysis, Resolution microscopy, Simultaneous staining, Single intraperitoneal injection, Sinusoid, Stagnant leukocytes, Uorescence, Uorescence microscopy, Uorescent latex particles, Vivo analysis, Vivo microscopy, Vollmar, Zonal distribution.
Abstract
Aim: There is strong evidence that hepatocellular apoptosis is not only initiated by circulating blood cells which become adherent within the endotoxemic liver, but also contributes to further sustain the inflammatory cell–cell response.
Methods: Because previous studies assumed the importance of the role of cellular cross‐talk in mediating inflammatory liver injury, we herein examined the activation of Kupffer cells (KCs) and their spatial coincidence with intrahepatic leukocyte adherence and hepatocellular apoptosis at 6 h after intraperitoneal exposure of rats with lipopolysaccharide (10 mg/kg).
Results: In vivo multifluorescence microscopy revealed liver injury including nutritive perfusion failure, tissue hypoxia, leukocyte accumulation, as well as KC activation and parenchymal apoptotic cell death. Detailed spatial analysis revealed frequent colocalization of activated KCs with apoptotic hepatocytes. Colocalization was absent in saline‐treated controls.Colocalization was confirmed by histochemistry, which showed ED1‐positive KCs neighboring and engulfing TUNEL‐positive hepatocytes. Colocalization of KCs with leukocytes ranged between 4% and 5% and did not increase in endotoxemic animals. Taken together, the present results indicate that apoptotic cell death of hepatocytes may stimulate phagocytosis by neighboring KCs. Direct KC–leukocyte contact seems not to be mandatory for cellular communication in the process of hepatocellular apoptosis.
Conclusion: With respect to the fundamental importance of cell apoptosis, improved knowledge of these cell–cell interactions might allow the development of new therapeutic strategies through the regulation of apoptotic cell death.
Url:
DOI: 10.1111/j.1872-034X.2007.00133.x
Affiliations:
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Menger</name></author><author><name sortKey="Vollmar, Brigitte" sort="Vollmar, Brigitte" uniqKey="Vollmar B" first="Brigitte" last="Vollmar">Brigitte Vollmar</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:AFDB71A6F806FF8E7593FC83915BC03E73791CB2</idno><date when="2007" year="2007">2007</date><idno type="doi">10.1111/j.1872-034X.2007.00133.x</idno><idno type="url">https://api.istex.fr/document/AFDB71A6F806FF8E7593FC83915BC03E73791CB2/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001236</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001236</idno><idno type="wicri:Area/Istex/Curation">001147</idno><idno type="wicri:Area/Istex/Checkpoint">000664</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000664</idno><idno type="wicri:doubleKey">1386-6346:2007:Eipel C:local:interaction:of</idno><idno type="wicri:Area/Main/Merge">000850</idno><idno type="wicri:Area/Main/Curation">000850</idno><idno type="wicri:Area/Main/Exploration">000850</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Local interaction of apoptotic hepatocytes and Kupffer cells in a rat model of systemic endotoxemia</title><author><name sortKey="Eipel, Christian" sort="Eipel, Christian" uniqKey="Eipel C" first="Christian" last="Eipel">Christian Eipel</name><affiliation></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Allemagne</country></affiliation></author><author><name sortKey="Hirschmann, Martin" sort="Hirschmann, Martin" uniqKey="Hirschmann M" first="Martin" last="Hirschmann">Martin Hirschmann</name><affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Abshagen, Kerstin" sort="Abshagen, Kerstin" uniqKey="Abshagen K" first="Kerstin" last="Abshagen">Kerstin Abshagen</name><affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Menger, Michael D" sort="Menger, Michael D" uniqKey="Menger M" first="Michael D." last="Menger">Michael D. Menger</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Clinical & Experimental Surgery, University of Saarland, Homburg‐Saar</wicri:regionArea><wicri:noRegion>Homburg‐Saar</wicri:noRegion><wicri:noRegion>Homburg‐Saar</wicri:noRegion></affiliation></author><author><name sortKey="Vollmar, Brigitte" sort="Vollmar, Brigitte" uniqKey="Vollmar B" first="Brigitte" last="Vollmar">Brigitte Vollmar</name><affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Hepatology Research</title><idno type="ISSN">1386-6346</idno><idno type="eISSN">1872-034X</idno><imprint><publisher>Blackwell Publishing Asia</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2007-10">2007-10</date><biblScope unit="volume">37</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="863">863</biblScope><biblScope unit="page" to="871">871</biblScope></imprint><idno type="ISSN">1386-6346</idno></series><idno type="istex">AFDB71A6F806FF8E7593FC83915BC03E73791CB2</idno><idno type="DOI">10.1111/j.1872-034X.2007.00133.x</idno><idno type="ArticleID">HEPR133</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1386-6346</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>colocalization</term><term>intravital fluorescence microscopy</term><term>lipopolysaccharide</term><term>liver</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Adherent</term><term>Adherent latex particles</term><term>Apoptosis</term><term>Apoptotic</term><term>Apoptotic bodies</term><term>Apoptotic cell death</term><term>Apoptotic hepatocytes</term><term>Coli</term><term>Colocalization</term><term>Control animals</term><term>Direct vicinity</term><term>Eipel</term><term>Endotoxemic</term><term>Endotoxemic animals</term><term>Equivalent volume</term><term>Experimental surgery</term><term>Gadolinium chloride</term><term>Hepatic</term><term>Hepatocellular</term><term>Hepatocellular apoptosis</term><term>Hepatocyte apoptosis</term><term>Hepatocytes</term><term>Hepatology</term><term>Hepatology hepatology research</term><term>Hepatology research</term><term>Intraperitoneal</term><term>Intravital</term><term>Isotonic saline</term><term>Japan society</term><term>Kupffer</term><term>Kupffer cells</term><term>Latex</term><term>Latex particles</term><term>Leukocyte</term><term>Liver injury</term><term>Liver tissue</term><term>Macrophage</term><term>Menger</term><term>Observation period</term><term>Parenchymal</term><term>Physiol</term><term>Platelet</term><term>Postsinusoidal venules</term><term>Quantitative analysis</term><term>Resolution microscopy</term><term>Simultaneous staining</term><term>Single intraperitoneal injection</term><term>Sinusoid</term><term>Stagnant leukocytes</term><term>Uorescence</term><term>Uorescence microscopy</term><term>Uorescent latex particles</term><term>Vivo analysis</term><term>Vivo microscopy</term><term>Vollmar</term><term>Zonal distribution</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Aim: There is strong evidence that hepatocellular apoptosis is not only initiated by circulating blood cells which become adherent within the endotoxemic liver, but also contributes to further sustain the inflammatory cell–cell response.</div><div type="abstract">Methods: Because previous studies assumed the importance of the role of cellular cross‐talk in mediating inflammatory liver injury, we herein examined the activation of Kupffer cells (KCs) and their spatial coincidence with intrahepatic leukocyte adherence and hepatocellular apoptosis at 6 h after intraperitoneal exposure of rats with lipopolysaccharide (10 mg/kg).</div><div type="abstract">Results: In vivo multifluorescence microscopy revealed liver injury including nutritive perfusion failure, tissue hypoxia, leukocyte accumulation, as well as KC activation and parenchymal apoptotic cell death. Detailed spatial analysis revealed frequent colocalization of activated KCs with apoptotic hepatocytes. Colocalization was absent in saline‐treated controls.Colocalization was confirmed by histochemistry, which showed ED1‐positive KCs neighboring and engulfing TUNEL‐positive hepatocytes. Colocalization of KCs with leukocytes ranged between 4% and 5% and did not increase in endotoxemic animals. Taken together, the present results indicate that apoptotic cell death of hepatocytes may stimulate phagocytosis by neighboring KCs. Direct KC–leukocyte contact seems not to be mandatory for cellular communication in the process of hepatocellular apoptosis.</div><div type="abstract">Conclusion: With respect to the fundamental importance of cell apoptosis, improved knowledge of these cell–cell interactions might allow the development of new therapeutic strategies through the regulation of apoptotic cell death.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country></list><tree><noCountry><name sortKey="Abshagen, Kerstin" sort="Abshagen, Kerstin" uniqKey="Abshagen K" first="Kerstin" last="Abshagen">Kerstin Abshagen</name><name sortKey="Hirschmann, Martin" sort="Hirschmann, Martin" uniqKey="Hirschmann M" first="Martin" last="Hirschmann">Martin Hirschmann</name><name sortKey="Vollmar, Brigitte" sort="Vollmar, Brigitte" uniqKey="Vollmar B" first="Brigitte" last="Vollmar">Brigitte Vollmar</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Eipel, Christian" sort="Eipel, Christian" uniqKey="Eipel C" first="Christian" last="Eipel">Christian Eipel</name></noRegion><name sortKey="Menger, Michael D" sort="Menger, Michael D" uniqKey="Menger M" first="Michael D." last="Menger">Michael D. Menger</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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