Impaired lymphatic contraction associated with immunosuppression.
Identifieur interne : 002399 ( PubMed/Corpus ); précédent : 002398; suivant : 002400Impaired lymphatic contraction associated with immunosuppression.
Auteurs : Shan Liao ; Gang Cheng ; David A. Conner ; Yuhui Huang ; Raju S. Kucherlapati ; Lance L. Munn ; Nancy H. Ruddle ; Rakesh K. Jain ; Dai Fukumura ; Timothy P. PaderaSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2011.
English descriptors
- KwdEn :
- Animals, Antigens, CD11b (biosynthesis), Bone Marrow Cells (cytology), Immune System, Immunosuppression, Inflammation, Kinetics, Lymphatic Metastasis, Lymphatic System (physiology), Lymphatic Vessels (drug effects), Lymphatic Vessels (pathology), Mice, Mice, Inbred C57BL, Microscopy (methods), Nitric Oxide Synthase Type III (metabolism), Oxazolone (pharmacology), Skin (drug effects).
- MESH :
- chemical , biosynthesis : Antigens, CD11b.
- cytology : Bone Marrow Cells.
- drug effects : Lymphatic Vessels, Skin.
- chemical , metabolism : Nitric Oxide Synthase Type III.
- methods : Microscopy.
- pathology : Lymphatic Vessels.
- chemical , pharmacology : Oxazolone.
- physiology : Lymphatic System.
- Animals, Immune System, Immunosuppression, Inflammation, Kinetics, Lymphatic Metastasis, Mice, Mice, Inbred C57BL.
Abstract
To trigger an effective immune response, antigen and antigen-presenting cells travel to the lymph nodes via collecting lymphatic vessels. However, our understanding of the regulation of collecting lymphatic vessel function and lymph transport is limited. To dissect the molecular control of lymphatic function, we developed a unique mouse model that allows intravital imaging of autonomous lymphatic vessel contraction. Using this method, we demonstrated that endothelial nitric oxide synthase (eNOS) in lymphatic endothelial cells is required for robust lymphatic contractions under physiological conditions. By contrast, under inflammatory conditions, inducible NOS (iNOS)-expressing CD11b(+)Gr-1(+) cells attenuate lymphatic contraction. This inhibition of lymphatic contraction was associated with a reduction in the response to antigen in a model of immune-induced multiple sclerosis. These results suggest the suppression of lymphatic function by the CD11b(+)Gr-1(+) cells as a potential mechanism of self-protection from autoreactive responses during on-going inflammation. The central role for nitric oxide also suggests that other diseases such as cancer and infection may also mediate lymphatic contraction and thus immune response. Our unique method allows the study of lymphatic function and its molecular regulation during inflammation, lymphedema, and lymphatic metastasis.
DOI: 10.1073/pnas.1116152108
PubMed: 22065738
Links to Exploration step
pubmed:22065738Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Impaired lymphatic contraction associated with immunosuppression.</title><author><name sortKey="Liao, Shan" sort="Liao, Shan" uniqKey="Liao S" first="Shan" last="Liao">Shan Liao</name><affiliation><nlm:affiliation>EL Steele Laboratory, Department of Radiation Oncology, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02114, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cheng, Gang" sort="Cheng, Gang" uniqKey="Cheng G" first="Gang" last="Cheng">Gang Cheng</name></author><author><name sortKey="Conner, David A" sort="Conner, David A" uniqKey="Conner D" first="David A" last="Conner">David A. Conner</name></author><author><name sortKey="Huang, Yuhui" sort="Huang, Yuhui" uniqKey="Huang Y" first="Yuhui" last="Huang">Yuhui Huang</name></author><author><name sortKey="Kucherlapati, Raju S" sort="Kucherlapati, Raju S" uniqKey="Kucherlapati R" first="Raju S" last="Kucherlapati">Raju S. Kucherlapati</name></author><author><name sortKey="Munn, Lance L" sort="Munn, Lance L" uniqKey="Munn L" first="Lance L" last="Munn">Lance L. Munn</name></author><author><name sortKey="Ruddle, Nancy H" sort="Ruddle, Nancy H" uniqKey="Ruddle N" first="Nancy H" last="Ruddle">Nancy H. Ruddle</name></author><author><name sortKey="Jain, Rakesh K" sort="Jain, Rakesh K" uniqKey="Jain R" first="Rakesh K" last="Jain">Rakesh K. Jain</name></author><author><name sortKey="Fukumura, Dai" sort="Fukumura, Dai" uniqKey="Fukumura D" first="Dai" last="Fukumura">Dai Fukumura</name></author><author><name sortKey="Padera, Timothy P" sort="Padera, Timothy P" uniqKey="Padera T" first="Timothy P" last="Padera">Timothy P. 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Conner</name></author><author><name sortKey="Huang, Yuhui" sort="Huang, Yuhui" uniqKey="Huang Y" first="Yuhui" last="Huang">Yuhui Huang</name></author><author><name sortKey="Kucherlapati, Raju S" sort="Kucherlapati, Raju S" uniqKey="Kucherlapati R" first="Raju S" last="Kucherlapati">Raju S. Kucherlapati</name></author><author><name sortKey="Munn, Lance L" sort="Munn, Lance L" uniqKey="Munn L" first="Lance L" last="Munn">Lance L. Munn</name></author><author><name sortKey="Ruddle, Nancy H" sort="Ruddle, Nancy H" uniqKey="Ruddle N" first="Nancy H" last="Ruddle">Nancy H. Ruddle</name></author><author><name sortKey="Jain, Rakesh K" sort="Jain, Rakesh K" uniqKey="Jain R" first="Rakesh K" last="Jain">Rakesh K. Jain</name></author><author><name sortKey="Fukumura, Dai" sort="Fukumura, Dai" uniqKey="Fukumura D" first="Dai" last="Fukumura">Dai Fukumura</name></author><author><name sortKey="Padera, Timothy P" sort="Padera, Timothy P" uniqKey="Padera T" first="Timothy P" last="Padera">Timothy P. Padera</name></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, CD11b (biosynthesis)</term><term>Bone Marrow Cells (cytology)</term><term>Immune System</term><term>Immunosuppression</term><term>Inflammation</term><term>Kinetics</term><term>Lymphatic Metastasis</term><term>Lymphatic System (physiology)</term><term>Lymphatic Vessels (drug effects)</term><term>Lymphatic Vessels (pathology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Microscopy (methods)</term><term>Nitric Oxide Synthase Type III (metabolism)</term><term>Oxazolone (pharmacology)</term><term>Skin (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Antigens, CD11b</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Bone Marrow Cells</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lymphatic Vessels</term><term>Skin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nitric Oxide Synthase Type III</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Microscopy</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Oxazolone</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphatic System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Immune System</term><term>Immunosuppression</term><term>Inflammation</term><term>Kinetics</term><term>Lymphatic Metastasis</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To trigger an effective immune response, antigen and antigen-presenting cells travel to the lymph nodes via collecting lymphatic vessels. However, our understanding of the regulation of collecting lymphatic vessel function and lymph transport is limited. To dissect the molecular control of lymphatic function, we developed a unique mouse model that allows intravital imaging of autonomous lymphatic vessel contraction. Using this method, we demonstrated that endothelial nitric oxide synthase (eNOS) in lymphatic endothelial cells is required for robust lymphatic contractions under physiological conditions. By contrast, under inflammatory conditions, inducible NOS (iNOS)-expressing CD11b(+)Gr-1(+) cells attenuate lymphatic contraction. This inhibition of lymphatic contraction was associated with a reduction in the response to antigen in a model of immune-induced multiple sclerosis. These results suggest the suppression of lymphatic function by the CD11b(+)Gr-1(+) cells as a potential mechanism of self-protection from autoreactive responses during on-going inflammation. The central role for nitric oxide also suggests that other diseases such as cancer and infection may also mediate lymphatic contraction and thus immune response. Our unique method allows the study of lymphatic function and its molecular regulation during inflammation, lymphedema, and lymphatic metastasis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22065738</PMID><DateCreated><Year>2011</Year><Month>11</Month><Day>17</Day></DateCreated><DateCompleted><Year>2012</Year><Month>01</Month><Day>26</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>108</Volume><Issue>46</Issue><PubDate><Year>2011</Year><Month>Nov</Month><Day>15</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>Impaired lymphatic contraction associated with immunosuppression.</ArticleTitle><Pagination><MedlinePgn>18784-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.1116152108</ELocationID><Abstract><AbstractText>To trigger an effective immune response, antigen and antigen-presenting cells travel to the lymph nodes via collecting lymphatic vessels. However, our understanding of the regulation of collecting lymphatic vessel function and lymph transport is limited. To dissect the molecular control of lymphatic function, we developed a unique mouse model that allows intravital imaging of autonomous lymphatic vessel contraction. Using this method, we demonstrated that endothelial nitric oxide synthase (eNOS) in lymphatic endothelial cells is required for robust lymphatic contractions under physiological conditions. By contrast, under inflammatory conditions, inducible NOS (iNOS)-expressing CD11b(+)Gr-1(+) cells attenuate lymphatic contraction. This inhibition of lymphatic contraction was associated with a reduction in the response to antigen in a model of immune-induced multiple sclerosis. These results suggest the suppression of lymphatic function by the CD11b(+)Gr-1(+) cells as a potential mechanism of self-protection from autoreactive responses during on-going inflammation. The central role for nitric oxide also suggests that other diseases such as cancer and infection may also mediate lymphatic contraction and thus immune response. Our unique method allows the study of lymphatic function and its molecular regulation during inflammation, lymphedema, and lymphatic metastasis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liao</LastName><ForeName>Shan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>EL Steele Laboratory, Department of Radiation Oncology, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02114, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Gang</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Conner</LastName><ForeName>David A</ForeName><Initials>DA</Initials></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Yuhui</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Kucherlapati</LastName><ForeName>Raju S</ForeName><Initials>RS</Initials></Author><Author ValidYN="Y"><LastName>Munn</LastName><ForeName>Lance L</ForeName><Initials>LL</Initials></Author><Author ValidYN="Y"><LastName>Ruddle</LastName><ForeName>Nancy H</ForeName><Initials>NH</Initials></Author><Author ValidYN="Y"><LastName>Jain</LastName><ForeName>Rakesh K</ForeName><Initials>RK</Initials></Author><Author ValidYN="Y"><LastName>Fukumura</LastName><ForeName>Dai</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Padera</LastName><ForeName>Timothy P</ForeName><Initials>TP</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01-CA96915</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA126642</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 CA084301</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R00 CA137167</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA085140</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-CA115767</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01-CA80124</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 CA080124</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-CA126642</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K99-CA137167</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK057731</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01-CA084301</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-CA85140</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA115767</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA096915</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK57731</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K99 CA137167</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>11</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D039481">Antigens, CD11b</NameOfSubstance></Chemical><Chemical><RegistryNumber>15646-46-5</RegistryNumber><NameOfSubstance UI="D010081">Oxazolone</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="D052250">Nitric Oxide Synthase Type III</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol. 1999 Dec;277(6 Pt 2):R1683-9</RefSource><PMID 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MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008853" MajorTopicYN="N">Microscopy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052250" MajorTopicYN="N">Nitric Oxide Synthase Type III</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010081" MajorTopicYN="N">Oxazolone</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012867" MajorTopicYN="N">Skin</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3219138</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>1</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22065738</ArticleId><ArticleId IdType="pii">1116152108</ArticleId><ArticleId IdType="doi">10.1073/pnas.1116152108</ArticleId><ArticleId 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