Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation.
Identifieur interne : 003D98 ( PubMed/Corpus ); précédent : 003D97; suivant : 003D99Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation.
Auteurs : Peter Baluk ; Tuomas Tammela ; Erin Ator ; Natalya Lyubynska ; Marc G. Achen ; Daniel J. Hicklin ; Michael Jeltsch ; Tatiana V. Petrova ; Bronislaw Pytowski ; Steven A. Stacker ; Seppo Yl Herttuala ; David G. Jackson ; Kari Alitalo ; Donald M. McdonaldSource :
- The Journal of clinical investigation [ 0021-9738 ] ; 2005.
English descriptors
- KwdEn :
- Adenoviridae, Airway Obstruction, Animals, Bronchi (blood supply), Bronchi (metabolism), Bronchi (microbiology), Bronchi (pathology), Chronic Disease, Dendritic Cells (metabolism), Dendritic Cells (pathology), Endothelial Growth Factors, Gene Expression Regulation (genetics), Hyperplasia (microbiology), Hyperplasia (pathology), Inflammation (genetics), Inflammation (metabolism), Inflammation (microbiology), Inflammation (pathology), Lymph Nodes (metabolism), Lymph Nodes (pathology), Lymphatic Vessels (metabolism), Lymphatic Vessels (pathology), Macrophages, Alveolar (metabolism), Macrophages, Alveolar (pathology), Mice, Mice, Inbred C3H, Mycoplasma Infections (metabolism), Mycoplasma Infections (pathology), Mycoplasma pulmonis, Neovascularization, Pathologic (genetics), Neovascularization, Pathologic (metabolism), Neovascularization, Pathologic (microbiology), Neovascularization, Pathologic (pathology), Neutrophils (metabolism), Neutrophils (pathology), Pulmonary Edema (genetics), Pulmonary Edema (microbiology), Pulmonary Edema (pathology), Respiratory Mucosa (metabolism), Respiratory Mucosa (microbiology), Respiratory Mucosa (pathology), Signal Transduction (genetics), Vascular Endothelial Growth Factor C (genetics), Vascular Endothelial Growth Factor C (metabolism), Vascular Endothelial Growth Factor D (genetics), Vascular Endothelial Growth Factor D (metabolism).
- MESH :
- chemical , genetics : Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor D.
- chemical , metabolism : Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor D.
- chemical : Endothelial Growth Factors.
- blood supply : Bronchi.
- genetics : Gene Expression Regulation, Inflammation, Neovascularization, Pathologic, Pulmonary Edema, Signal Transduction.
- metabolism : Bronchi, Dendritic Cells, Inflammation, Lymph Nodes, Lymphatic Vessels, Macrophages, Alveolar, Mycoplasma Infections, Neovascularization, Pathologic, Neutrophils, Respiratory Mucosa.
- microbiology : Bronchi, Hyperplasia, Inflammation, Neovascularization, Pathologic, Pulmonary Edema, Respiratory Mucosa.
- pathology : Bronchi, Dendritic Cells, Hyperplasia, Inflammation, Lymph Nodes, Lymphatic Vessels, Macrophages, Alveolar, Mycoplasma Infections, Neovascularization, Pathologic, Neutrophils, Pulmonary Edema, Respiratory Mucosa.
- Adenoviridae, Airway Obstruction, Animals, Chronic Disease, Mice, Mice, Inbred C3H, Mycoplasma pulmonis.
Abstract
Edema occurs in asthma and other inflammatory diseases when the rate of plasma leakage from blood vessels exceeds the drainage through lymphatic vessels and other routes. It is unclear to what extent lymphatic vessels grow to compensate for increased leakage during inflammation and what drives the lymphangiogenesis that does occur. We addressed these issues in mouse models of (a) chronic respiratory tract infection with Mycoplasma pulmonis and (b) adenoviral transduction of airway epithelium with VEGF family growth factors. Blood vessel remodeling and lymphangiogenesis were both robust in infected airways. Inhibition of VEGFR-3 signaling completely prevented the growth of lymphatic vessels but not blood vessels. Lack of lymphatic growth exaggerated mucosal edema and reduced the hypertrophy of draining lymph nodes. Airway dendritic cells, macrophages, neutrophils, and epithelial cells expressed the VEGFR-3 ligands VEGF-C or VEGF-D. Adenoviral delivery of either VEGF-C or VEGF-D evoked lymphangiogenesis without angiogenesis, whereas adenoviral VEGF had the opposite effect. After antibiotic treatment of the infection, inflammation and remodeling of blood vessels quickly subsided, but lymphatic vessels persisted. Together, these findings suggest that when lymphangiogenesis is impaired, airway inflammation may lead to bronchial lymphedema and exaggerated airflow obstruction. Correction of defective lymphangiogenesis may benefit the treatment of asthma and other inflammatory airway diseases.
DOI: 10.1172/JCI22037
PubMed: 15668734
Links to Exploration step
pubmed:15668734Le document en format XML
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Achen</name></author><author><name sortKey="Hicklin, Daniel J" sort="Hicklin, Daniel J" uniqKey="Hicklin D" first="Daniel J" last="Hicklin">Daniel J. Hicklin</name></author><author><name sortKey="Jeltsch, Michael" sort="Jeltsch, Michael" uniqKey="Jeltsch M" first="Michael" last="Jeltsch">Michael Jeltsch</name></author><author><name sortKey="Petrova, Tatiana V" sort="Petrova, Tatiana V" uniqKey="Petrova T" first="Tatiana V" last="Petrova">Tatiana V. Petrova</name></author><author><name sortKey="Pytowski, Bronislaw" sort="Pytowski, Bronislaw" uniqKey="Pytowski B" first="Bronislaw" last="Pytowski">Bronislaw Pytowski</name></author><author><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A" last="Stacker">Steven A. 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Achen</name></author><author><name sortKey="Hicklin, Daniel J" sort="Hicklin, Daniel J" uniqKey="Hicklin D" first="Daniel J" last="Hicklin">Daniel J. Hicklin</name></author><author><name sortKey="Jeltsch, Michael" sort="Jeltsch, Michael" uniqKey="Jeltsch M" first="Michael" last="Jeltsch">Michael Jeltsch</name></author><author><name sortKey="Petrova, Tatiana V" sort="Petrova, Tatiana V" uniqKey="Petrova T" first="Tatiana V" last="Petrova">Tatiana V. Petrova</name></author><author><name sortKey="Pytowski, Bronislaw" sort="Pytowski, Bronislaw" uniqKey="Pytowski B" first="Bronislaw" last="Pytowski">Bronislaw Pytowski</name></author><author><name sortKey="Stacker, Steven A" sort="Stacker, Steven A" uniqKey="Stacker S" first="Steven A" last="Stacker">Steven A. Stacker</name></author><author><name sortKey="Yl Herttuala, Seppo" sort="Yl Herttuala, Seppo" uniqKey="Yl Herttuala S" first="Seppo" last="Yl Herttuala">Seppo Yl Herttuala</name></author><author><name sortKey="Jackson, David G" sort="Jackson, David G" uniqKey="Jackson D" first="David G" last="Jackson">David G. Jackson</name></author><author><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name></author><author><name sortKey="Mcdonald, Donald M" sort="Mcdonald, Donald M" uniqKey="Mcdonald D" first="Donald M" last="Mcdonald">Donald M. Mcdonald</name></author></analytic><series><title level="j">The Journal of clinical investigation</title><idno type="ISSN">0021-9738</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenoviridae</term><term>Airway Obstruction</term><term>Animals</term><term>Bronchi (blood supply)</term><term>Bronchi (metabolism)</term><term>Bronchi (microbiology)</term><term>Bronchi (pathology)</term><term>Chronic Disease</term><term>Dendritic Cells (metabolism)</term><term>Dendritic Cells (pathology)</term><term>Endothelial Growth Factors</term><term>Gene Expression Regulation (genetics)</term><term>Hyperplasia (microbiology)</term><term>Hyperplasia (pathology)</term><term>Inflammation (genetics)</term><term>Inflammation (metabolism)</term><term>Inflammation (microbiology)</term><term>Inflammation (pathology)</term><term>Lymph Nodes (metabolism)</term><term>Lymph Nodes (pathology)</term><term>Lymphatic Vessels (metabolism)</term><term>Lymphatic Vessels (pathology)</term><term>Macrophages, Alveolar (metabolism)</term><term>Macrophages, Alveolar (pathology)</term><term>Mice</term><term>Mice, Inbred C3H</term><term>Mycoplasma Infections (metabolism)</term><term>Mycoplasma Infections (pathology)</term><term>Mycoplasma pulmonis</term><term>Neovascularization, Pathologic (genetics)</term><term>Neovascularization, Pathologic (metabolism)</term><term>Neovascularization, Pathologic (microbiology)</term><term>Neovascularization, Pathologic (pathology)</term><term>Neutrophils (metabolism)</term><term>Neutrophils (pathology)</term><term>Pulmonary Edema (genetics)</term><term>Pulmonary Edema (microbiology)</term><term>Pulmonary Edema (pathology)</term><term>Respiratory Mucosa (metabolism)</term><term>Respiratory Mucosa (microbiology)</term><term>Respiratory Mucosa (pathology)</term><term>Signal Transduction (genetics)</term><term>Vascular Endothelial Growth Factor C (genetics)</term><term>Vascular Endothelial Growth Factor C (metabolism)</term><term>Vascular Endothelial Growth Factor D (genetics)</term><term>Vascular Endothelial Growth Factor D (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor D</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Vascular Endothelial Growth Factor C</term><term>Vascular Endothelial Growth Factor D</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Endothelial Growth Factors</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Bronchi</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Expression Regulation</term><term>Inflammation</term><term>Neovascularization, Pathologic</term><term>Pulmonary Edema</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Bronchi</term><term>Dendritic Cells</term><term>Inflammation</term><term>Lymph Nodes</term><term>Lymphatic Vessels</term><term>Macrophages, Alveolar</term><term>Mycoplasma Infections</term><term>Neovascularization, Pathologic</term><term>Neutrophils</term><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Bronchi</term><term>Hyperplasia</term><term>Inflammation</term><term>Neovascularization, Pathologic</term><term>Pulmonary Edema</term><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Bronchi</term><term>Dendritic Cells</term><term>Hyperplasia</term><term>Inflammation</term><term>Lymph Nodes</term><term>Lymphatic Vessels</term><term>Macrophages, Alveolar</term><term>Mycoplasma Infections</term><term>Neovascularization, Pathologic</term><term>Neutrophils</term><term>Pulmonary Edema</term><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adenoviridae</term><term>Airway Obstruction</term><term>Animals</term><term>Chronic Disease</term><term>Mice</term><term>Mice, Inbred C3H</term><term>Mycoplasma pulmonis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Edema occurs in asthma and other inflammatory diseases when the rate of plasma leakage from blood vessels exceeds the drainage through lymphatic vessels and other routes. It is unclear to what extent lymphatic vessels grow to compensate for increased leakage during inflammation and what drives the lymphangiogenesis that does occur. We addressed these issues in mouse models of (a) chronic respiratory tract infection with Mycoplasma pulmonis and (b) adenoviral transduction of airway epithelium with VEGF family growth factors. Blood vessel remodeling and lymphangiogenesis were both robust in infected airways. Inhibition of VEGFR-3 signaling completely prevented the growth of lymphatic vessels but not blood vessels. Lack of lymphatic growth exaggerated mucosal edema and reduced the hypertrophy of draining lymph nodes. Airway dendritic cells, macrophages, neutrophils, and epithelial cells expressed the VEGFR-3 ligands VEGF-C or VEGF-D. Adenoviral delivery of either VEGF-C or VEGF-D evoked lymphangiogenesis without angiogenesis, whereas adenoviral VEGF had the opposite effect. After antibiotic treatment of the infection, inflammation and remodeling of blood vessels quickly subsided, but lymphatic vessels persisted. Together, these findings suggest that when lymphangiogenesis is impaired, airway inflammation may lead to bronchial lymphedema and exaggerated airflow obstruction. Correction of defective lymphangiogenesis may benefit the treatment of asthma and other inflammatory airway diseases.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15668734</PMID><DateCreated><Year>2005</Year><Month>02</Month><Day>03</Day></DateCreated><DateCompleted><Year>2005</Year><Month>03</Month><Day>23</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0021-9738</ISSN><JournalIssue CitedMedium="Print"><Volume>115</Volume><Issue>2</Issue><PubDate><Year>2005</Year><Month>Feb</Month></PubDate></JournalIssue><Title>The Journal of clinical investigation</Title><ISOAbbreviation>J. Clin. Invest.</ISOAbbreviation></Journal><ArticleTitle>Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation.</ArticleTitle><Pagination><MedlinePgn>247-57</MedlinePgn></Pagination><Abstract><AbstractText>Edema occurs in asthma and other inflammatory diseases when the rate of plasma leakage from blood vessels exceeds the drainage through lymphatic vessels and other routes. It is unclear to what extent lymphatic vessels grow to compensate for increased leakage during inflammation and what drives the lymphangiogenesis that does occur. We addressed these issues in mouse models of (a) chronic respiratory tract infection with Mycoplasma pulmonis and (b) adenoviral transduction of airway epithelium with VEGF family growth factors. Blood vessel remodeling and lymphangiogenesis were both robust in infected airways. Inhibition of VEGFR-3 signaling completely prevented the growth of lymphatic vessels but not blood vessels. Lack of lymphatic growth exaggerated mucosal edema and reduced the hypertrophy of draining lymph nodes. Airway dendritic cells, macrophages, neutrophils, and epithelial cells expressed the VEGFR-3 ligands VEGF-C or VEGF-D. Adenoviral delivery of either VEGF-C or VEGF-D evoked lymphangiogenesis without angiogenesis, whereas adenoviral VEGF had the opposite effect. After antibiotic treatment of the infection, inflammation and remodeling of blood vessels quickly subsided, but lymphatic vessels persisted. Together, these findings suggest that when lymphangiogenesis is impaired, airway inflammation may lead to bronchial lymphedema and exaggerated airflow obstruction. Correction of defective lymphangiogenesis may benefit the treatment of asthma and other inflammatory airway diseases.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Baluk</LastName><ForeName>Peter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Comprehensive Cancer Center, and Department of Anatomy, UCSF, San Francisco, California 94143, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tammela</LastName><ForeName>Tuomas</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Ator</LastName><ForeName>Erin</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Lyubynska</LastName><ForeName>Natalya</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Achen</LastName><ForeName>Marc G</ForeName><Initials>MG</Initials></Author><Author ValidYN="Y"><LastName>Hicklin</LastName><ForeName>Daniel J</ForeName><Initials>DJ</Initials></Author><Author ValidYN="Y"><LastName>Jeltsch</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Petrova</LastName><ForeName>Tatiana V</ForeName><Initials>TV</Initials></Author><Author ValidYN="Y"><LastName>Pytowski</LastName><ForeName>Bronislaw</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Stacker</LastName><ForeName>Steven A</ForeName><Initials>SA</Initials></Author><Author ValidYN="Y"><LastName>Ylä-Herttuala</LastName><ForeName>Seppo</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Jackson</LastName><ForeName>David G</ForeName><Initials>DG</Initials></Author><Author ValidYN="Y"><LastName>Alitalo</LastName><ForeName>Kari</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>McDonald</LastName><ForeName>Donald M</ForeName><Initials>DM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HL-24136</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 HL024136</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HD037243</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL059157</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL-59157</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Clin Invest</MedlineTA><NlmUniqueID>7802877</NlmUniqueID><ISSNLinking>0021-9738</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016228">Endothelial Growth Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042582">Vascular Endothelial Growth Factor C</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042643">Vascular Endothelial Growth Factor D</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Cancer Res. 1999 Oct 15;59(20):5209-18</RefSource><PMID Version="1">10537299</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am Rev Respir Dis. 1992 Jun;145(6):1251-8</RefSource><PMID 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PubStatus="accepted"><Year>2004</Year><Month>11</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>1</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>3</Month><Day>24</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>1</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15668734</ArticleId><ArticleId IdType="doi">10.1172/JCI22037</ArticleId><ArticleId IdType="pmc">PMC544601</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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