Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies
Identifieur interne : 000453 ( Istex/Corpus ); précédent : 000452; suivant : 000454Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies
Auteurs : Dirk J. Van Der Windt ; Rita Bottino ; Anna Casu ; Nathalie Campanile ; David K. C. CooperSource :
- Xenotransplantation [ 0908-665X ] ; 2007-07.
English descriptors
- KwdEn :
- Apoptosis, Clinical islet transplantation, Coagulation, Cytokine, Dextran, Diabetic mice, Early graft loss, Euglycemia, Graft, Human islets, Human pancreatic islets, Ibmir, Intraportal, Intraportal islet, Islet, Islet transplantation, Kidney capsule, Macrophage, Monocyte, Neutrophil, Overexpression, Pancreatic, Pathway, Platelet, Platelet activation, Porcine, Rapid loss, Sulfate, Thrombin, Tissue factor, Transplant, Transplantation, Xenotransplantation.
- Teeft :
- Apoptosis, Clinical islet transplantation, Coagulation, Cytokine, Dextran, Diabetic mice, Early graft loss, Euglycemia, Graft, Human islets, Human pancreatic islets, Ibmir, Intraportal, Intraportal islet, Islet, Islet transplantation, Kidney capsule, Macrophage, Monocyte, Neutrophil, Overexpression, Pancreatic, Pathway, Platelet, Platelet activation, Porcine, Rapid loss, Sulfate, Thrombin, Tissue factor, Transplant, Transplantation, Xenotransplantation.
Abstract
Abstract: Islets isolated from multiple pancreas donors are often necessary to achieve euglycemia in type 1 diabetic patients treated by islet allotransplantation. This increases the burden on the limited pool of donor organs. After infusion into the portal vein, a substantial percentage of islets are lost in the immediate post‐transplant period through an inflammatory response termed the instant blood‐mediated inflammatory reaction (IBMIR). IBMIR is equally, if not more of a problem after islet xenotransplantation, e.g., using pig islets in non‐human primates. Coagulation, platelet aggregation, complement activation, and neutrophil and monocyte infiltration play roles in this reaction. IBMIR is potentially triggered by islet surface molecules, such as tissue factor and collagen residues that are normally not in direct contact with the blood. Also, stress during the islet isolation process results in the expression and production of several inflammatory mediators by the islets themselves. The potential mechanisms involved in this rapid graft loss and treatment options to reduce this loss are reviewed. Preventive strategies for IBMIR can include systemic treatment of the recipient, pre‐conditioning of the isolated islets, or, in the case of xenotransplantation, genetic modification of the organ‐source pig. Pre‐conditioning of islets in culture by exposure to anti‐inflammatory agents or by genetic modification harbors fewer risks of systemic complications in the recipient. The future of clinical islet transplantation will, at least in part, depend on the success of efforts made to reduce rapid graft loss, and thus allow islet transplantation to become a more efficient therapy by the use of single donors.
Url:
DOI: 10.1111/j.1399-3089.2007.00419.x
Links to Exploration step
ISTEX:13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies</title><author><name sortKey="Van Der Windt, Dirk J" sort="Van Der Windt, Dirk J" uniqKey="Van Der Windt D" first="Dirk J." last="Van Der Windt">Dirk J. Van Der Windt</name><affiliation><mods:affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</mods:affiliation></affiliation><affiliation><mods:affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author><author><name sortKey="Bottino, Rita" sort="Bottino, Rita" uniqKey="Bottino R" first="Rita" last="Bottino">Rita Bottino</name><affiliation><mods:affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</mods:affiliation></affiliation></author><author><name sortKey="Casu, Anna" sort="Casu, Anna" uniqKey="Casu A" first="Anna" last="Casu">Anna Casu</name><affiliation><mods:affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</mods:affiliation></affiliation></author><author><name sortKey="Campanile, Nathalie" sort="Campanile, Nathalie" uniqKey="Campanile N" first="Nathalie" last="Campanile">Nathalie Campanile</name><affiliation><mods:affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</mods:affiliation></affiliation><affiliation><mods:affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author><author><name sortKey="Cooper, David K C" sort="Cooper, David K C" uniqKey="Cooper D" first="David K. C." last="Cooper">David K. C. Cooper</name><affiliation><mods:affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53</idno><date when="2007" year="2007">2007</date><idno type="doi">10.1111/j.1399-3089.2007.00419.x</idno><idno type="url">https://api.istex.fr/document/13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000453</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000453</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies</title><author><name sortKey="Van Der Windt, Dirk J" sort="Van Der Windt, Dirk J" uniqKey="Van Der Windt D" first="Dirk J." last="Van Der Windt">Dirk J. Van Der Windt</name><affiliation><mods:affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</mods:affiliation></affiliation><affiliation><mods:affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author><author><name sortKey="Bottino, Rita" sort="Bottino, Rita" uniqKey="Bottino R" first="Rita" last="Bottino">Rita Bottino</name><affiliation><mods:affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</mods:affiliation></affiliation></author><author><name sortKey="Casu, Anna" sort="Casu, Anna" uniqKey="Casu A" first="Anna" last="Casu">Anna Casu</name><affiliation><mods:affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</mods:affiliation></affiliation></author><author><name sortKey="Campanile, Nathalie" sort="Campanile, Nathalie" uniqKey="Campanile N" first="Nathalie" last="Campanile">Nathalie Campanile</name><affiliation><mods:affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</mods:affiliation></affiliation><affiliation><mods:affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author><author><name sortKey="Cooper, David K C" sort="Cooper, David K C" uniqKey="Cooper D" first="David K. C." last="Cooper">David K. C. Cooper</name><affiliation><mods:affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Xenotransplantation</title><title level="j" type="alt">XENOTRANSPLANTATION</title><idno type="ISSN">0908-665X</idno><idno type="eISSN">1399-3089</idno><imprint><biblScope unit="vol">14</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="288">288</biblScope><biblScope unit="page" to="297">297</biblScope><biblScope unit="page-count">10</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2007-07">2007-07</date></imprint><idno type="ISSN">0908-665X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0908-665X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term><term>Clinical islet transplantation</term><term>Coagulation</term><term>Cytokine</term><term>Dextran</term><term>Diabetic mice</term><term>Early graft loss</term><term>Euglycemia</term><term>Graft</term><term>Human islets</term><term>Human pancreatic islets</term><term>Ibmir</term><term>Intraportal</term><term>Intraportal islet</term><term>Islet</term><term>Islet transplantation</term><term>Kidney capsule</term><term>Macrophage</term><term>Monocyte</term><term>Neutrophil</term><term>Overexpression</term><term>Pancreatic</term><term>Pathway</term><term>Platelet</term><term>Platelet activation</term><term>Porcine</term><term>Rapid loss</term><term>Sulfate</term><term>Thrombin</term><term>Tissue factor</term><term>Transplant</term><term>Transplantation</term><term>Xenotransplantation</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Apoptosis</term><term>Clinical islet transplantation</term><term>Coagulation</term><term>Cytokine</term><term>Dextran</term><term>Diabetic mice</term><term>Early graft loss</term><term>Euglycemia</term><term>Graft</term><term>Human islets</term><term>Human pancreatic islets</term><term>Ibmir</term><term>Intraportal</term><term>Intraportal islet</term><term>Islet</term><term>Islet transplantation</term><term>Kidney capsule</term><term>Macrophage</term><term>Monocyte</term><term>Neutrophil</term><term>Overexpression</term><term>Pancreatic</term><term>Pathway</term><term>Platelet</term><term>Platelet activation</term><term>Porcine</term><term>Rapid loss</term><term>Sulfate</term><term>Thrombin</term><term>Tissue factor</term><term>Transplant</term><term>Transplantation</term><term>Xenotransplantation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Abstract: Islets isolated from multiple pancreas donors are often necessary to achieve euglycemia in type 1 diabetic patients treated by islet allotransplantation. This increases the burden on the limited pool of donor organs. After infusion into the portal vein, a substantial percentage of islets are lost in the immediate post‐transplant period through an inflammatory response termed the instant blood‐mediated inflammatory reaction (IBMIR). IBMIR is equally, if not more of a problem after islet xenotransplantation, e.g., using pig islets in non‐human primates. Coagulation, platelet aggregation, complement activation, and neutrophil and monocyte infiltration play roles in this reaction. IBMIR is potentially triggered by islet surface molecules, such as tissue factor and collagen residues that are normally not in direct contact with the blood. Also, stress during the islet isolation process results in the expression and production of several inflammatory mediators by the islets themselves. The potential mechanisms involved in this rapid graft loss and treatment options to reduce this loss are reviewed. Preventive strategies for IBMIR can include systemic treatment of the recipient, pre‐conditioning of the isolated islets, or, in the case of xenotransplantation, genetic modification of the organ‐source pig. Pre‐conditioning of islets in culture by exposure to anti‐inflammatory agents or by genetic modification harbors fewer risks of systemic complications in the recipient. The future of clinical islet transplantation will, at least in part, depend on the success of efforts made to reduce rapid graft loss, and thus allow islet transplantation to become a more efficient therapy by the use of single donors.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>islet</json:string><json:string>transplantation</json:string><json:string>ibmir</json:string><json:string>coagulation</json:string><json:string>pathway</json:string><json:string>platelet</json:string><json:string>porcine</json:string><json:string>pancreatic</json:string><json:string>euglycemia</json:string><json:string>thrombin</json:string><json:string>xenotransplantation</json:string><json:string>intraportal</json:string><json:string>apoptosis</json:string><json:string>islet transplantation</json:string><json:string>human islets</json:string><json:string>cytokine</json:string><json:string>overexpression</json:string><json:string>neutrophil</json:string><json:string>graft</json:string><json:string>macrophage</json:string><json:string>diabetic mice</json:string><json:string>sulfate</json:string><json:string>dextran</json:string><json:string>clinical islet transplantation</json:string><json:string>kidney capsule</json:string><json:string>monocyte</json:string><json:string>rapid loss</json:string><json:string>tissue factor</json:string><json:string>platelet activation</json:string><json:string>intraportal islet</json:string><json:string>early graft loss</json:string><json:string>human pancreatic islets</json:string><json:string>transplant</json:string><json:string>dextran sulfate</json:string><json:string>tubing loops model</json:string><json:string>clinical trials</json:string><json:string>islet mass</json:string><json:string>clinical islet</json:string><json:string>portal vein</json:string><json:string>diabetes</json:string><json:string>diabetic</json:string><json:string>human blood</json:string><json:string>diabetic patients</json:string><json:string>complement activation</json:string><json:string>instant reaction</json:string><json:string>oxidative stress</json:string><json:string>human serum cytotoxicity</json:string><json:string>whole blood</json:string><json:string>systemic treatment</json:string><json:string>intrinsic pathway</json:string><json:string>superoxide dismutase</json:string><json:string>glutathione peroxidase</json:string><json:string>oxygen radicals</json:string><json:string>carbon monoxide</json:string><json:string>collagen residues</json:string><json:string>preventive strategies</json:string><json:string>neutrophilic granulocytes</json:string><json:string>inhibitor</json:string></teeft></keywords><author><json:item><name>Dirk J. Van Der Windt</name><affiliations><json:string>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</json:string><json:string>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</json:string></affiliations></json:item><json:item><name>Rita Bottino</name><affiliations><json:string>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</json:string></affiliations></json:item><json:item><name>Anna Casu</name><affiliations><json:string>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</json:string></affiliations></json:item><json:item><name>Nathalie Campanile</name><affiliations><json:string>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</json:string><json:string>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</json:string></affiliations></json:item><json:item><name>David K.C. Cooper</name><affiliations><json:string>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>coagulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>complement</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>instant blood‐mediated inflammatory reaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>islets of Langerhans</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>platelets</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>transplantation</value></json:item></subject><articleId><json:string>XEN419</json:string></articleId><arkIstex>ark:/67375/WNG-0KNTPBQ9-3</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>reviewArticle</json:string></originalGenre><abstract>Abstract: Islets isolated from multiple pancreas donors are often necessary to achieve euglycemia in type 1 diabetic patients treated by islet allotransplantation. This increases the burden on the limited pool of donor organs. After infusion into the portal vein, a substantial percentage of islets are lost in the immediate post‐transplant period through an inflammatory response termed the instant blood‐mediated inflammatory reaction (IBMIR). IBMIR is equally, if not more of a problem after islet xenotransplantation, e.g., using pig islets in non‐human primates. Coagulation, platelet aggregation, complement activation, and neutrophil and monocyte infiltration play roles in this reaction. IBMIR is potentially triggered by islet surface molecules, such as tissue factor and collagen residues that are normally not in direct contact with the blood. Also, stress during the islet isolation process results in the expression and production of several inflammatory mediators by the islets themselves. The potential mechanisms involved in this rapid graft loss and treatment options to reduce this loss are reviewed. Preventive strategies for IBMIR can include systemic treatment of the recipient, pre‐conditioning of the isolated islets, or, in the case of xenotransplantation, genetic modification of the organ‐source pig. Pre‐conditioning of islets in culture by exposure to anti‐inflammatory agents or by genetic modification harbors fewer risks of systemic complications in the recipient. The future of clinical islet transplantation will, at least in part, depend on the success of efforts made to reduce rapid graft loss, and thus allow islet transplantation to become a more efficient therapy by the use of single donors.</abstract><qualityIndicators><score>10</score><pdfWordCount>6033</pdfWordCount><pdfCharCount>41421</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>251</abstractWordCount><abstractCharCount>1732</abstractCharCount><keywordCount>6</keywordCount></qualityIndicators><title>Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies</title><pmid><json:string>17669170</json:string></pmid><genre><json:string>review-article</json:string></genre><host><title>Xenotransplantation</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1399-3089</json:string></doi><issn><json:string>0908-665X</json:string></issn><eissn><json:string>1399-3089</json:string></eissn><publisherId><json:string>XEN</json:string></publisherId><volume>14</volume><issue>4</issue><pages><first>288</first><last>297</last><total>10</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2007</json:string></date><geogName></geogName><orgName><json:string>Revivicor, Inc.</json:string><json:string>Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA Key</json:string><json:string>Department of Defense Grant</json:string><json:string>University of Pittsburgh</json:string><json:string>American Diabetes Association Grant</json:string><json:string>Juvenile Diabetes Research Foundation Grant</json:string><json:string>Sponsored Research Agreement</json:string><json:string>Hospital of Pittsburgh</json:string><json:string>Starzl Transplantation Institute, University of Pittsburgh Medical Center, Biomedical Science Tower</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Mechanism</json:string><json:string>Anna Casu</json:string><json:string>Nathalie Campanile</json:string><json:string>In</json:string><json:string>K.C. Cooper</json:string><json:string>Professor Massimo</json:string><json:string>D.K.C. Cooper</json:string><json:string>Rita Bottino</json:string></persName><placeName><json:string>Edmonton</json:string><json:string>Pittsburgh</json:string><json:string>PA</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[61]</json:string><json:string>[4]</json:string><json:string>[67]</json:string><json:string>[29]</json:string><json:string>[6]</json:string><json:string>[71]</json:string><json:string>[66]</json:string><json:string>[53,54]</json:string><json:string>[46,63]</json:string><json:string>[8]</json:string><json:string>[28]</json:string><json:string>[47,48]</json:string><json:string>[40,45]</json:string><json:string>[37,60]</json:string><json:string>[65]</json:string><json:string>[49]</json:string><json:string>[3]</json:string><json:string>[80]</json:string><json:string>[4,36]</json:string><json:string>[64]</json:string><json:string>[5]</json:string><json:string>[59]</json:string><json:string>[62,63]</json:string><json:string>[15,36]</json:string><json:string>[6,18,19]</json:string><json:string>[67,68]</json:string><json:string>[36,51]</json:string><json:string>[69,70]</json:string><json:string>[74]</json:string><json:string>[7]</json:string><json:string>[58]</json:string><json:string>[72,73]</json:string><json:string>[9]</json:string><json:string>[62]</json:string><json:string>[77,78]</json:string><json:string>van der Windt et al.</json:string><json:string>[2]</json:string><json:string>[68]</json:string><json:string>[19]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-0KNTPBQ9-3</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - transplantation</json:string><json:string>2 - medicine, research & experimental</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - surgery</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Transplantation</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Immunology</json:string></scopus></categories><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1111/j.1399-3089.2007.00419.x</json:string></doi><id>13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2007-07"></date></publicationStmt><notesStmt><note type="content-type" subtype="review-article" source="reviewArticle" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="review-article"><analytic><title level="a" type="main">Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies</title><title level="a" type="short">Rapid loss of transplanted islets</title><author xml:id="author-0000"><persName><forename type="first">Dirk J.</forename><surname>Van Der Windt</surname></persName><affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</affiliation><affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Rita</forename><surname>Bottino</surname></persName><affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Anna</forename><surname>Casu</surname></persName><affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Nathalie</forename><surname>Campanile</surname></persName><affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</affiliation><affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">David K.C.</forename><surname>Cooper</surname></persName><affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA<address><country key="US"></country></address></affiliation></author><idno type="istex">13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53</idno><idno type="ark">ark:/67375/WNG-0KNTPBQ9-3</idno><idno type="DOI">10.1111/j.1399-3089.2007.00419.x</idno><idno type="unit">XEN419</idno><idno type="toTypesetVersion">file:XEN.XEN419.pdf</idno></analytic><monogr><title level="j" type="main">Xenotransplantation</title><title level="j" type="alt">XENOTRANSPLANTATION</title><idno type="pISSN">0908-665X</idno><idno type="eISSN">1399-3089</idno><idno type="book-DOI">10.1111/(ISSN)1399-3089</idno><idno type="book-part-DOI">10.1111/xen.2007.14.issue-4</idno><idno type="product">XEN</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">14</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="288">288</biblScope><biblScope unit="page" to="297">297</biblScope><biblScope unit="page-count">10</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2007-07"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">Abstract: </hi> Islets isolated from multiple pancreas donors are often necessary to achieve euglycemia in type 1 diabetic patients treated by islet allotransplantation. This increases the burden on the limited pool of donor organs. After infusion into the portal vein, a substantial percentage of islets are lost in the immediate post‐transplant period through an inflammatory response termed the instant blood‐mediated inflammatory reaction (IBMIR). IBMIR is equally, if not more of a problem after islet xenotransplantation, e.g., using pig islets in non‐human primates. Coagulation, platelet aggregation, complement activation, and neutrophil and monocyte infiltration play roles in this reaction. IBMIR is potentially triggered by islet surface molecules, such as tissue factor and collagen residues that are normally not in direct contact with the blood. Also, stress during the islet isolation process results in the expression and production of several inflammatory mediators by the islets themselves. The potential mechanisms involved in this rapid graft loss and treatment options to reduce this loss are reviewed. Preventive strategies for IBMIR can include systemic treatment of the recipient, pre‐conditioning of the isolated islets, or, in the case of xenotransplantation, genetic modification of the organ‐source pig. Pre‐conditioning of islets in culture by exposure to anti‐inflammatory agents or by genetic modification harbors fewer risks of systemic complications in the recipient. The future of clinical islet transplantation will, at least in part, depend on the success of efforts made to reduce rapid graft loss, and thus allow islet transplantation to become a more efficient therapy by the use of single donors.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">coagulation</term><term xml:id="k2">complement</term><term xml:id="k3">instant blood‐mediated inflammatory reaction</term><term xml:id="k4">islets of Langerhans</term><term xml:id="k5">platelets</term><term xml:id="k6">transplantation</term></keywords><keywords rend="tocHeading1"><term>Review Article</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1399-3089</doi><issn type="print">0908-665X</issn><issn type="electronic">1399-3089</issn><idGroup><id type="product" value="XEN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="XENOTRANSPLANTATION">Xenotransplantation</title></titleGroup></publicationMeta><publicationMeta level="part" position="07004"><doi origin="wiley">10.1111/xen.2007.14.issue-4</doi><numberingGroup><numbering type="journalVolume" number="14">14</numbering><numbering type="journalIssue" number="4">4</numbering></numberingGroup><coverDate startDate="2007-07">July 2007</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="4" status="forIssue"><doi origin="wiley">10.1111/j.1399-3089.2007.00419.x</doi><idGroup><id type="unit" value="XEN419"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="tocHeading1">R<sc>eview</sc> A<sc>rticle</sc></title></titleGroup><eventGroup><event type="firstOnline" date="2007-07-28"></event><event type="publishedOnlineFinalForm" date="2007-07-28"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-10"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="288">288</numbering><numbering type="pageLast" number="297">297</numbering></numberingGroup><correspondenceTo>Address reprint requests to D.K.C. Cooper, MD, PhD, FRCS, Thomas E. Starzl Transplantation Institute, University of Pittsburgh Medical Center, Biomedical Science Tower, W1543, 200 Lothrop Street, Pittsburgh, PA 15261, USA
(E‐mail: <email>cooperdk@upmc.edu</email>)</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:XEN.XEN419.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 18 June 2007; Accepted 26 June 2007</unparsedEditorialHistory><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="3"></count></countGroup><titleGroup><title type="main">Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies</title><title type="shortAuthors"><b>van der Windt et al.</b></title><title type="short"><b>Rapid loss of transplanted islets</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>Dirk J.</givenNames><familyName>Van Der Windt</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Rita</givenNames><familyName>Bottino</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Anna</givenNames><familyName>Casu</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1 #a2"><personName><givenNames>Nathalie</givenNames><familyName>Campanile</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a2"><personName><givenNames>David K.C.</givenNames><familyName>Cooper</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">coagulation</keyword><keyword xml:id="k2">complement</keyword><keyword xml:id="k3">instant blood‐mediated inflammatory reaction</keyword><keyword xml:id="k4">islets of Langerhans</keyword><keyword xml:id="k5">platelets</keyword><keyword xml:id="k6">transplantation</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!--
van der Windt DJ, Bottino R, Casu A, Campanile N, Cooper DKC. Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies.
Xenotransplantation 2007; 14: 288–297. © Blackwell Munksgaard, 2007
--><p><b>Abstract: </b> Islets isolated from multiple pancreas donors are often necessary to achieve euglycemia in type 1 diabetic patients treated by islet allotransplantation. This increases the burden on the limited pool of donor organs. After infusion into the portal vein, a substantial percentage of islets are lost in the immediate post‐transplant period through an inflammatory response termed the instant blood‐mediated inflammatory reaction (IBMIR). IBMIR is equally, if not more of a problem after islet xenotransplantation, e.g., using pig islets in non‐human primates. Coagulation, platelet aggregation, complement activation, and neutrophil and monocyte infiltration play roles in this reaction. IBMIR is potentially triggered by islet surface molecules, such as tissue factor and collagen residues that are normally not in direct contact with the blood. Also, stress during the islet isolation process results in the expression and production of several inflammatory mediators by the islets themselves. The potential mechanisms involved in this rapid graft loss and treatment options to reduce this loss are reviewed. Preventive strategies for IBMIR can include systemic treatment of the recipient, pre‐conditioning of the isolated islets, or, in the case of xenotransplantation, genetic modification of the organ‐source pig. Pre‐conditioning of islets in culture by exposure to anti‐inflammatory agents or by genetic modification harbors fewer risks of systemic complications in the recipient. The future of clinical islet transplantation will, at least in part, depend on the success of efforts made to reduce rapid graft loss, and thus allow islet transplantation to become a more efficient therapy by the use of single donors.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Rapid loss of transplanted islets</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies</title></titleInfo><name type="personal"><namePart type="given">Dirk J.</namePart><namePart type="family">Van Der Windt</namePart><affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</affiliation><affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rita</namePart><namePart type="family">Bottino</namePart><affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anna</namePart><namePart type="family">Casu</namePart><affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nathalie</namePart><namePart type="family">Campanile</namePart><affiliation>Department of Pediatrics, Division of Immunogenetics, Children’s Hospital of Pittsburgh</affiliation><affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David K.C.</namePart><namePart type="family">Cooper</namePart><affiliation>Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2007-07</dateIssued><edition>Received 18 June 2007; Accepted 26 June 2007</edition><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">3</extent><extent unit="tables">3</extent></physicalDescription><abstract>Abstract: Islets isolated from multiple pancreas donors are often necessary to achieve euglycemia in type 1 diabetic patients treated by islet allotransplantation. This increases the burden on the limited pool of donor organs. After infusion into the portal vein, a substantial percentage of islets are lost in the immediate post‐transplant period through an inflammatory response termed the instant blood‐mediated inflammatory reaction (IBMIR). IBMIR is equally, if not more of a problem after islet xenotransplantation, e.g., using pig islets in non‐human primates. Coagulation, platelet aggregation, complement activation, and neutrophil and monocyte infiltration play roles in this reaction. IBMIR is potentially triggered by islet surface molecules, such as tissue factor and collagen residues that are normally not in direct contact with the blood. Also, stress during the islet isolation process results in the expression and production of several inflammatory mediators by the islets themselves. The potential mechanisms involved in this rapid graft loss and treatment options to reduce this loss are reviewed. Preventive strategies for IBMIR can include systemic treatment of the recipient, pre‐conditioning of the isolated islets, or, in the case of xenotransplantation, genetic modification of the organ‐source pig. Pre‐conditioning of islets in culture by exposure to anti‐inflammatory agents or by genetic modification harbors fewer risks of systemic complications in the recipient. The future of clinical islet transplantation will, at least in part, depend on the success of efforts made to reduce rapid graft loss, and thus allow islet transplantation to become a more efficient therapy by the use of single donors.</abstract><subject lang="en"><genre>keywords</genre><topic>coagulation</topic><topic>complement</topic><topic>instant blood‐mediated inflammatory reaction</topic><topic>islets of Langerhans</topic><topic>platelets</topic><topic>transplantation</topic></subject><relatedItem type="host"><titleInfo><title>Xenotransplantation</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0908-665X</identifier><identifier type="eISSN">1399-3089</identifier><identifier type="DOI">10.1111/(ISSN)1399-3089</identifier><identifier type="PublisherID">XEN</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>288</start><end>297</end><total>10</total></extent></part></relatedItem><identifier type="istex">13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53</identifier><identifier type="ark">ark:/67375/WNG-0KNTPBQ9-3</identifier><identifier type="DOI">10.1111/j.1399-3089.2007.00419.x</identifier><identifier type="ArticleID">XEN419</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Amérique/explor/PittsburghV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000453 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000453 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Amérique
|area= PittsburghV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:13385EC5FE4ADE6B25A5384F7E3C08EA04CA5C53
|texte= Rapid loss of intraportally transplanted islets: an overview of pathophysiology and preventive strategies
}}
| This area was generated with Dilib version V0.6.38. |  |