Conjugated primary bile salts reduce permeability of endotoxin through intestinal epithelial cells and synergize with phosphatidylcholine in suppression of inflammatory cytokine production
OBJECTIVE:Endotoxemia was shown to be integral in the pathophysiology of obstructive jaundice. In the current study, the role of conjugated primary bile salts (CPBS) and phosphatidylcholine on the permeability of endotoxin through a layer of intestinal epithelial cells and the consequent activation...
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| Veröffentlicht in: | Critical care medicine 2007-10, Vol.35 (10), p.2367-2374 |
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| creator | Parlesak, Alexandr Schaeckeler, Simone Moser, Lydia Bode, Christiane |
| description | OBJECTIVE:Endotoxemia was shown to be integral in the pathophysiology of obstructive jaundice. In the current study, the role of conjugated primary bile salts (CPBS) and phosphatidylcholine on the permeability of endotoxin through a layer of intestinal epithelial cells and the consequent activation of basolaterally cocultured human mononuclear leukocytes were measured.
DESIGN:In a coculture model, a layer of differentiated, confluent Caco-2 cells was apically stimulated with growth-arrested, nonpathogenic Escherichia coli.
SETTING:Basic human cell culture laboratory.
INTERVENTIONS:The effect of CPBS (0.5 mM and 1.5 mM), phosphatidylcholine (0.38 mM), and human bile (0.5% vol/vol) on the barrier function was assessed by the measurement of transepithelial electrical resistance, by endotoxin permeability through the intestinal epithelial cell layer, and by basolateral cytokine enzyme-linked immunosorbent assay measurement (tumor necrosis factor-α, interleukins-6, -8, and -10). Micelles formed by CPBS were detected by dynamic light scattering. The association of endotoxin with CPBS micelles was tested by fluorescence resonance energy transfer.
MEASUREMENTS AND MAIN RESULTS:Apical addition of CPBS suppressed the permeability of endotoxins through the intestinal epithelial cell layer significantly. In parallel, apical supplementation of CPBS dose-dependently reduced the basolateral production of all cytokines measured. Apical phosphatidylcholine supplementation enhanced this effect significantly. CPBS formed micelles (diameter, 134 ± 7 nm), which were able to bind endotoxin to their surface.
CONCLUSIONS:CPBS can reduce the permeation of endotoxin through intestinal epithelial cell layers by binding it to micelles. Thereby, the inflammatory processes beyond the mucosal surface are suppressed, an effect that is enhanced by phosphatidylcholine. |
| doi_str_mv | 10.1097/01.CCM.0000284586.84952.FB |
| format | Article |
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DESIGN:In a coculture model, a layer of differentiated, confluent Caco-2 cells was apically stimulated with growth-arrested, nonpathogenic Escherichia coli.
SETTING:Basic human cell culture laboratory.
INTERVENTIONS:The effect of CPBS (0.5 mM and 1.5 mM), phosphatidylcholine (0.38 mM), and human bile (0.5% vol/vol) on the barrier function was assessed by the measurement of transepithelial electrical resistance, by endotoxin permeability through the intestinal epithelial cell layer, and by basolateral cytokine enzyme-linked immunosorbent assay measurement (tumor necrosis factor-α, interleukins-6, -8, and -10). Micelles formed by CPBS were detected by dynamic light scattering. The association of endotoxin with CPBS micelles was tested by fluorescence resonance energy transfer.
MEASUREMENTS AND MAIN RESULTS:Apical addition of CPBS suppressed the permeability of endotoxins through the intestinal epithelial cell layer significantly. In parallel, apical supplementation of CPBS dose-dependently reduced the basolateral production of all cytokines measured. Apical phosphatidylcholine supplementation enhanced this effect significantly. CPBS formed micelles (diameter, 134 ± 7 nm), which were able to bind endotoxin to their surface.
CONCLUSIONS:CPBS can reduce the permeation of endotoxin through intestinal epithelial cell layers by binding it to micelles. Thereby, the inflammatory processes beyond the mucosal surface are suppressed, an effect that is enhanced by phosphatidylcholine.</description><identifier>ISSN: 0090-3493</identifier><identifier>EISSN: 1530-0293</identifier><identifier>DOI: 10.1097/01.CCM.0000284586.84952.FB</identifier><identifier>PMID: 17944028</identifier><identifier>CODEN: CCMDC7</identifier><language>eng</language><publisher>Hagerstown, MD: by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Bile Acids and Salts - physiology ; Biological and medical sciences ; Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis ; Bone marrow, stem cells transplantation. Graft versus host reaction ; Cells, Cultured ; Endotoxins - metabolism ; Humans ; Inflammation - immunology ; Inflammation - metabolism ; Intensive care medicine ; Interleukin-10 - biosynthesis ; Interleukin-6 - biosynthesis ; Interleukin-8 - biosynthesis ; Intestinal Mucosa - cytology ; Intestinal Mucosa - metabolism ; Medical sciences ; Permeability ; Phosphatidylcholines - physiology ; Transfusions. Complications. Transfusion reactions. Cell and gene therapy ; Tumor Necrosis Factor-alpha - biosynthesis</subject><ispartof>Critical care medicine, 2007-10, Vol.35 (10), p.2367-2374</ispartof><rights>2007 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</rights><rights>2007 INIST-CNRS</rights><rights>(C) 2007 Lippincott Williams & Wilkins, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5010-c0160c69d7bebaa581ee178c056e4bc7afc4bbc20dc96cfb4777e237c6aa45d93</citedby><cites>FETCH-LOGICAL-c5010-c0160c69d7bebaa581ee178c056e4bc7afc4bbc20dc96cfb4777e237c6aa45d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19121679$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17944028$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Parlesak, Alexandr</creatorcontrib><creatorcontrib>Schaeckeler, Simone</creatorcontrib><creatorcontrib>Moser, Lydia</creatorcontrib><creatorcontrib>Bode, Christiane</creatorcontrib><title>Conjugated primary bile salts reduce permeability of endotoxin through intestinal epithelial cells and synergize with phosphatidylcholine in suppression of inflammatory cytokine production</title><title>Critical care medicine</title><addtitle>Crit Care Med</addtitle><description>OBJECTIVE:Endotoxemia was shown to be integral in the pathophysiology of obstructive jaundice. In the current study, the role of conjugated primary bile salts (CPBS) and phosphatidylcholine on the permeability of endotoxin through a layer of intestinal epithelial cells and the consequent activation of basolaterally cocultured human mononuclear leukocytes were measured.
DESIGN:In a coculture model, a layer of differentiated, confluent Caco-2 cells was apically stimulated with growth-arrested, nonpathogenic Escherichia coli.
SETTING:Basic human cell culture laboratory.
INTERVENTIONS:The effect of CPBS (0.5 mM and 1.5 mM), phosphatidylcholine (0.38 mM), and human bile (0.5% vol/vol) on the barrier function was assessed by the measurement of transepithelial electrical resistance, by endotoxin permeability through the intestinal epithelial cell layer, and by basolateral cytokine enzyme-linked immunosorbent assay measurement (tumor necrosis factor-α, interleukins-6, -8, and -10). Micelles formed by CPBS were detected by dynamic light scattering. The association of endotoxin with CPBS micelles was tested by fluorescence resonance energy transfer.
MEASUREMENTS AND MAIN RESULTS:Apical addition of CPBS suppressed the permeability of endotoxins through the intestinal epithelial cell layer significantly. In parallel, apical supplementation of CPBS dose-dependently reduced the basolateral production of all cytokines measured. Apical phosphatidylcholine supplementation enhanced this effect significantly. CPBS formed micelles (diameter, 134 ± 7 nm), which were able to bind endotoxin to their surface.
CONCLUSIONS:CPBS can reduce the permeation of endotoxin through intestinal epithelial cell layers by binding it to micelles. Thereby, the inflammatory processes beyond the mucosal surface are suppressed, an effect that is enhanced by phosphatidylcholine.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Bile Acids and Salts - physiology</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis</subject><subject>Bone marrow, stem cells transplantation. Graft versus host reaction</subject><subject>Cells, Cultured</subject><subject>Endotoxins - metabolism</subject><subject>Humans</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Intensive care medicine</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Interleukin-8 - biosynthesis</subject><subject>Intestinal Mucosa - cytology</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Medical sciences</subject><subject>Permeability</subject><subject>Phosphatidylcholines - physiology</subject><subject>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0090-3493</issn><issn>1530-0293</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkc1u1DAUhSMEoqXwCshCgl2G68SJY3Z0xABSERtYR45zM3Hr2MF2NB2ejYfD6Yw03vjvu_cc-2TZOwobCoJ_BLrZbn9sII2iYVVTbxomqmKzu32WXdOqhBwKUT7PrgEE5CUT5VX2KoR7AMoqXr7MrigXjKXi6-zf1tn7ZS8j9mT2epL-SDptkARpYiAe-0UhmdFPKNO5jkfiBoK2d9E9akvi6N2yH4m2EUPUVhqCs44jGp2WCo0JRNqehKNFv9d_kRzSLZlHF-ZRRt0fjRqd0RZTCxKWefYYgnZ2ldF2MHKaZHTJlTpG97Bys3fJVEzM6-zFIE3AN-f5Jvu9-_Jr-y2_-_n1-_bzXa4qoJAroDWoWvS8w07KqqGIlDcKqhpZp7gcFOs6VUCvRK2GjnHOsSi5qqVkVS_Km-zDqW-S_rOkd7aTDuvbpEW3hLZuSsHrokjgpxOovAvB49Ce_7Sl0K7ZtUDblF17ya59yq7d3abit2eVpZuwv5Sew0rA-zMgg5Jm8NIqHS6coAWt-WqXnbiDMxF9eDDLAX07Yop0fJIuC1bnBQCn6y5fzUD5H6GSunE</recordid><startdate>200710</startdate><enddate>200710</enddate><creator>Parlesak, Alexandr</creator><creator>Schaeckeler, Simone</creator><creator>Moser, Lydia</creator><creator>Bode, Christiane</creator><general>by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</general><general>Lippincott</general><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>7X8</scope></search><sort><creationdate>200710</creationdate><title>Conjugated primary bile salts reduce permeability of endotoxin through intestinal epithelial cells and synergize with phosphatidylcholine in suppression of inflammatory cytokine production</title><author>Parlesak, Alexandr ; Schaeckeler, Simone ; Moser, Lydia ; Bode, Christiane</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5010-c0160c69d7bebaa581ee178c056e4bc7afc4bbc20dc96cfb4777e237c6aa45d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Bile Acids and Salts - physiology</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis</topic><topic>Bone marrow, stem cells transplantation. Graft versus host reaction</topic><topic>Cells, Cultured</topic><topic>Endotoxins - metabolism</topic><topic>Humans</topic><topic>Inflammation - immunology</topic><topic>Inflammation - metabolism</topic><topic>Intensive care medicine</topic><topic>Interleukin-10 - biosynthesis</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Interleukin-8 - biosynthesis</topic><topic>Intestinal Mucosa - cytology</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Medical sciences</topic><topic>Permeability</topic><topic>Phosphatidylcholines - physiology</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Parlesak, Alexandr</creatorcontrib><creatorcontrib>Schaeckeler, Simone</creatorcontrib><creatorcontrib>Moser, Lydia</creatorcontrib><creatorcontrib>Bode, Christiane</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Critical care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Parlesak, Alexandr</au><au>Schaeckeler, Simone</au><au>Moser, Lydia</au><au>Bode, Christiane</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Conjugated primary bile salts reduce permeability of endotoxin through intestinal epithelial cells and synergize with phosphatidylcholine in suppression of inflammatory cytokine production</atitle><jtitle>Critical care medicine</jtitle><addtitle>Crit Care Med</addtitle><date>2007-10</date><risdate>2007</risdate><volume>35</volume><issue>10</issue><spage>2367</spage><epage>2374</epage><pages>2367-2374</pages><issn>0090-3493</issn><eissn>1530-0293</eissn><coden>CCMDC7</coden><abstract>OBJECTIVE:Endotoxemia was shown to be integral in the pathophysiology of obstructive jaundice. In the current study, the role of conjugated primary bile salts (CPBS) and phosphatidylcholine on the permeability of endotoxin through a layer of intestinal epithelial cells and the consequent activation of basolaterally cocultured human mononuclear leukocytes were measured.
DESIGN:In a coculture model, a layer of differentiated, confluent Caco-2 cells was apically stimulated with growth-arrested, nonpathogenic Escherichia coli.
SETTING:Basic human cell culture laboratory.
INTERVENTIONS:The effect of CPBS (0.5 mM and 1.5 mM), phosphatidylcholine (0.38 mM), and human bile (0.5% vol/vol) on the barrier function was assessed by the measurement of transepithelial electrical resistance, by endotoxin permeability through the intestinal epithelial cell layer, and by basolateral cytokine enzyme-linked immunosorbent assay measurement (tumor necrosis factor-α, interleukins-6, -8, and -10). Micelles formed by CPBS were detected by dynamic light scattering. The association of endotoxin with CPBS micelles was tested by fluorescence resonance energy transfer.
MEASUREMENTS AND MAIN RESULTS:Apical addition of CPBS suppressed the permeability of endotoxins through the intestinal epithelial cell layer significantly. In parallel, apical supplementation of CPBS dose-dependently reduced the basolateral production of all cytokines measured. Apical phosphatidylcholine supplementation enhanced this effect significantly. CPBS formed micelles (diameter, 134 ± 7 nm), which were able to bind endotoxin to their surface.
CONCLUSIONS:CPBS can reduce the permeation of endotoxin through intestinal epithelial cell layers by binding it to micelles. Thereby, the inflammatory processes beyond the mucosal surface are suppressed, an effect that is enhanced by phosphatidylcholine.</abstract><cop>Hagerstown, MD</cop><pub>by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</pub><pmid>17944028</pmid><doi>10.1097/01.CCM.0000284586.84952.FB</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Critical care medicine, 2007-10, Vol.35 (10), p.2367-2374 |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Bile Acids and Salts - physiology Biological and medical sciences Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis Bone marrow, stem cells transplantation. Graft versus host reaction Cells, Cultured Endotoxins - metabolism Humans Inflammation - immunology Inflammation - metabolism Intensive care medicine Interleukin-10 - biosynthesis Interleukin-6 - biosynthesis Interleukin-8 - biosynthesis Intestinal Mucosa - cytology Intestinal Mucosa - metabolism Medical sciences Permeability Phosphatidylcholines - physiology Transfusions. Complications. Transfusion reactions. Cell and gene therapy Tumor Necrosis Factor-alpha - biosynthesis |
| title | Conjugated primary bile salts reduce permeability of endotoxin through intestinal epithelial cells and synergize with phosphatidylcholine in suppression of inflammatory cytokine production |
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