Blockade of VEGF receptor-3 aggravates inflammatory bowel disease and lymphatic vessel enlargement
Identifieur interne : 003852 ( Main/Exploration ); précédent : 003851; suivant : 003853Blockade of VEGF receptor-3 aggravates inflammatory bowel disease and lymphatic vessel enlargement
Auteurs : Giorgia Jurisic [Suisse] ; John P. Sundberg [États-Unis] ; Michael Detmar [Suisse]Source :
- Inflammatory bowel diseases [ 1078-0998 ] ; 2013.
Abstract
In contrast to the prominent function of the blood vasculature in promoting tissue inflammation, the role of lymphatic vessels in inflammation has been scarcely studied
Interleukin 10 (IL10)-deficient mice that spontaneously develop inflammatory bowel disease, were treated with a blocking antibody to VEGFR-3 for 2 weeks, and the inflammatory changes in colon tissue, as well as the blood and lymphatic vascularization were quantitatively analyzed.
We found a significant increase in the severity of colon inflammation in anti-VEGFR-3 treated mice. This was accompanied by an increased number of enlarged and tortuous lymphatic vessels, and edema in colon submucosa, indicating impaired lymphatic function. In contrast, no major effects of the treatment on the blood vasculature were observed.
These results indicate that therapies aimed at promoting lymphatic function, e.g., with pro-lymphangiogenic factors such as VEGF-C, might provide a novel strategy for the treatment of inflammatory conditions such as inflammatory bowel disease.
Url:
DOI: 10.1097/MIB.0b013e31829292f7
PubMed: 23835443
PubMed Central: 3732464
Affiliations:
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Sundberg</name><affiliation wicri:level="1"><nlm:aff id="A2">The Jackson Laboratory, Bar Harbor ME, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>The Jackson Laboratory, Bar Harbor ME</wicri:regionArea><wicri:noRegion>Bar Harbor ME</wicri:noRegion></affiliation></author><author><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name><affiliation wicri:level="1"><nlm:aff id="A1">Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland</nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich</wicri:regionArea><wicri:noRegion>8093 Zurich</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23835443</idno><idno type="pmc">3732464</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732464</idno><idno type="RBID">PMC:3732464</idno><idno type="doi">10.1097/MIB.0b013e31829292f7</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">003A35</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003A35</idno><idno type="wicri:Area/Pmc/Curation">003A34</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">003A34</idno><idno type="wicri:Area/Pmc/Checkpoint">002480</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">002480</idno><idno type="wicri:Area/Ncbi/Merge">005B11</idno><idno type="wicri:Area/Ncbi/Curation">005B11</idno><idno type="wicri:Area/Ncbi/Checkpoint">005B11</idno><idno type="wicri:doubleKey">1078-0998:2013:Jurisic G:blockade:of:vegf</idno><idno type="wicri:Area/Main/Merge">003860</idno><idno type="wicri:Area/Main/Curation">003852</idno><idno type="wicri:Area/Main/Exploration">003852</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Blockade of VEGF receptor-3 aggravates inflammatory bowel disease and lymphatic vessel enlargement</title><author><name sortKey="Jurisic, Giorgia" sort="Jurisic, Giorgia" uniqKey="Jurisic G" first="Giorgia" last="Jurisic">Giorgia Jurisic</name><affiliation wicri:level="1"><nlm:aff id="A1">Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland</nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich</wicri:regionArea><wicri:noRegion>8093 Zurich</wicri:noRegion></affiliation></author><author><name sortKey="Sundberg, John P" sort="Sundberg, John P" uniqKey="Sundberg J" first="John P" last="Sundberg">John P. Sundberg</name><affiliation wicri:level="1"><nlm:aff id="A2">The Jackson Laboratory, Bar Harbor ME, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>The Jackson Laboratory, Bar Harbor ME</wicri:regionArea><wicri:noRegion>Bar Harbor ME</wicri:noRegion></affiliation></author><author><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name><affiliation wicri:level="1"><nlm:aff id="A1">Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland</nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich</wicri:regionArea><wicri:noRegion>8093 Zurich</wicri:noRegion></affiliation></author></analytic><series><title level="j">Inflammatory bowel diseases</title><idno type="ISSN">1078-0998</idno><idno type="eISSN">1536-4844</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title><p id="P2">In contrast to the prominent function of the blood vasculature in promoting tissue inflammation, the role of lymphatic vessels in inflammation has been scarcely studied <italic>in vivo</italic>. To investigate whether modulating lymphatic vessel function might affect the course of chronic inflammation the major lymphangiogenic receptor vascular growth factor receptor 3 (VEGFR-3, FLT4) was blocked in an established model of inflammatory bowel disease.</p></sec><sec id="S2"><title>Methods</title><p id="P3">Interleukin 10 (IL10)-deficient mice that spontaneously develop inflammatory bowel disease, were treated with a blocking antibody to VEGFR-3 for 2 weeks, and the inflammatory changes in colon tissue, as well as the blood and lymphatic vascularization were quantitatively analyzed.</p></sec><sec id="S3"><title>Results</title><p id="P4">We found a significant increase in the severity of colon inflammation in anti-VEGFR-3 treated mice. This was accompanied by an increased number of enlarged and tortuous lymphatic vessels, and edema in colon submucosa, indicating impaired lymphatic function. In contrast, no major effects of the treatment on the blood vasculature were observed.</p></sec><sec id="S4"><title>Conclusions</title><p id="P5">These results indicate that therapies aimed at promoting lymphatic function, e.g., with pro-lymphangiogenic factors such as VEGF-C, might provide a novel strategy for the treatment of inflammatory conditions such as inflammatory bowel disease.</p></sec></div></front></TEI><affiliations><list><country><li>Suisse</li><li>États-Unis</li></country></list><tree><country name="Suisse"><noRegion><name sortKey="Jurisic, Giorgia" sort="Jurisic, Giorgia" uniqKey="Jurisic G" first="Giorgia" last="Jurisic">Giorgia Jurisic</name></noRegion><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name></country><country name="États-Unis"><noRegion><name sortKey="Sundberg, John P" sort="Sundberg, John P" uniqKey="Sundberg J" first="John P" last="Sundberg">John P. Sundberg</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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