Inflammatory Manifestations of Lymphedema
Identifieur interne : 000238 ( Pmc/Checkpoint ); précédent : 000237; suivant : 000239Inflammatory Manifestations of Lymphedema
Auteurs : Catherine L. Ly ; Raghu P. Kataru ; Babak J. MehraraSource :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2017.
Abstract
Lymphedema results from lymphatic insufficiency leading to a progressive inflammatory process that ultimately manifests as discomfort, recurrent infections, and, at times, secondary malignancy. Collectively, these morbidities contribute to an overall poor quality of life. Although there have been recent advances in microsurgical interventions, a conservative palliative approach remains the mainstay of treatment for this disabling disease. The absence of a cure is due to an incomplete understanding of the pathophysiological changes that result in lymphedema. A histological hallmark of lymphedema is inflammatory cell infiltration and recent studies with animal models and clinical biopsy specimens have suggested that this response plays a key role in the pathology of the disease. The purpose of this report is to provide an overview of the ongoing research in and the current understanding of the inflammatory manifestations of lymphedema.
Url:
DOI: 10.3390/ijms18010171
PubMed: 28106728
PubMed Central: 5297803
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Inflammatory Manifestations of Lymphedema</title><author><name sortKey="Ly, Catherine L" sort="Ly, Catherine L" uniqKey="Ly C" first="Catherine L." last="Ly">Catherine L. Ly</name></author><author><name sortKey="Kataru, Raghu P" sort="Kataru, Raghu P" uniqKey="Kataru R" first="Raghu P." last="Kataru">Raghu P. Kataru</name></author><author><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J." last="Mehrara">Babak J. Mehrara</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">28106728</idno><idno type="pmc">5297803</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5297803</idno><idno type="RBID">PMC:5297803</idno><idno type="doi">10.3390/ijms18010171</idno><date when="2017">2017</date><idno type="wicri:Area/Pmc/Corpus">004A75</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">004A75</idno><idno type="wicri:Area/Pmc/Curation">004A74</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">004A74</idno><idno type="wicri:Area/Pmc/Checkpoint">000238</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000238</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Inflammatory Manifestations of Lymphedema</title><author><name sortKey="Ly, Catherine L" sort="Ly, Catherine L" uniqKey="Ly C" first="Catherine L." last="Ly">Catherine L. Ly</name></author><author><name sortKey="Kataru, Raghu P" sort="Kataru, Raghu P" uniqKey="Kataru R" first="Raghu P." last="Kataru">Raghu P. Kataru</name></author><author><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J." last="Mehrara">Babak J. Mehrara</name></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</idno><imprint><date when="2017">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Lymphedema results from lymphatic insufficiency leading to a progressive inflammatory process that ultimately manifests as discomfort, recurrent infections, and, at times, secondary malignancy. Collectively, these morbidities contribute to an overall poor quality of life. Although there have been recent advances in microsurgical interventions, a conservative palliative approach remains the mainstay of treatment for this disabling disease. The absence of a cure is due to an incomplete understanding of the pathophysiological changes that result in lymphedema. A histological hallmark of lymphedema is inflammatory cell infiltration and recent studies with animal models and clinical biopsy specimens have suggested that this response plays a key role in the pathology of the disease. The purpose of this report is to provide an overview of the ongoing research in and the current understanding of the inflammatory manifestations of lymphedema.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Warren, A G" uniqKey="Warren A">A.G. Warren</name></author><author><name sortKey="Brorson, H" uniqKey="Brorson H">H. Brorson</name></author><author><name sortKey="Borud, L J" uniqKey="Borud L">L.J. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Mol Sci</journal-id><journal-id journal-id-type="iso-abbrev">Int J Mol Sci</journal-id><journal-id journal-id-type="publisher-id">ijms</journal-id><journal-title-group><journal-title>International Journal of Molecular Sciences</journal-title></journal-title-group><issn pub-type="epub">1422-0067</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">28106728</article-id><article-id pub-id-type="pmc">5297803</article-id><article-id pub-id-type="doi">10.3390/ijms18010171</article-id><article-id pub-id-type="publisher-id">ijms-18-00171</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Inflammatory Manifestations of Lymphedema</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Ly</surname><given-names>Catherine L.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Kataru</surname><given-names>Raghu P.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Mehrara</surname><given-names>Babak J.</given-names></name><xref rid="c1-ijms-18-00171" ref-type="corresp">*</xref></contrib></contrib-group><contrib-group><contrib contrib-type="editor"><name><surname>Jackson</surname><given-names>Chris</given-names></name><role>Academic Editor</role></contrib></contrib-group><aff id="af1-ijms-18-00171">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA;<email>lyc@mskcc.org</email> (C.L.L.);<email>katarur@mskcc.org</email> (R.P.K.)</aff><author-notes><corresp id="c1-ijms-18-00171"><label>*</label>Correspondence: <email>mehrarab@mskcc.org</email>; Tel.: +1-212-639-8639; Fax: +1-212-717-3677</corresp></author-notes><pub-date pub-type="epub"><day>17</day><month>1</month><year>2017</year></pub-date><pub-date pub-type="collection"><month>1</month><year>2017</year></pub-date><volume>18</volume><issue>1</issue><elocation-id>171</elocation-id><history><date date-type="received"><day>25</day><month>10</month><year>2016</year></date><date date-type="accepted"><day>12</day><month>1</month><year>2017</year></date></history><permissions><copyright-statement>© 2017 by the authors; licensee MDPI, Basel, Switzerland.</copyright-statement><copyright-year>2017</copyright-year><license><license-p><pmc-comment>CREATIVE COMMONS</pmc-comment>This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Lymphedema results from lymphatic insufficiency leading to a progressive inflammatory process that ultimately manifests as discomfort, recurrent infections, and, at times, secondary malignancy. Collectively, these morbidities contribute to an overall poor quality of life. Although there have been recent advances in microsurgical interventions, a conservative palliative approach remains the mainstay of treatment for this disabling disease. The absence of a cure is due to an incomplete understanding of the pathophysiological changes that result in lymphedema. A histological hallmark of lymphedema is inflammatory cell infiltration and recent studies with animal models and clinical biopsy specimens have suggested that this response plays a key role in the pathology of the disease. The purpose of this report is to provide an overview of the ongoing research in and the current understanding of the inflammatory manifestations of lymphedema.</p></abstract><kwd-group><kwd>lymphedema</kwd><kwd>inflammatory skin conditions</kwd><kwd>inflammatory cells</kwd><kwd>immunity</kwd></kwd-group></article-meta></front><floats-group><fig id="ijms-18-00171-f001" position="float"><label>Figure 1</label><caption><p>Mouse models of lymphedema. (<bold>A</bold>) Tail surgery model, in which the lymphatics are ligated after circumferential full-thickness skin excision and identification with blue dye. Note the increase in fibroadipose thickness and inflammation following lymphatic injury; inflammatory cells are indicated by the brown color; (<bold>B</bold>) Popliteal lymph node dissection (PLND) model, similar to the axillary lymph node dissection (ALND) model, in which the appropriate lymph node is removed with its corresponding fat pad (as indicated by the blue arrow). This model is particularly useful for evaluation of collecting vessel pumping, collateral lymphatic formation, and dendritic cell (DC) trafficking, all of which are decreased following lymphadenectomy. In the left panel, note the decreased frequency of collecting vessel pumping as indicated by the black line graphs (each peak represents one pump; arbitrary units) and the paucity of patent collecting lymphatic vessels as indicated by absence of distinct vessels highlighted by the red/orange dye in mice that had undergone lymphadenectomy compared to control mice. Lymphatic injury also prevents transport of mature DCs to lymph nodes, where they would initiate immune responses; (<bold>C</bold>) Diphtheria toxin-mediated lymphatic ablation model, in which human diphtheria toxin receptor is coupled with lymphatic-specific receptor promoter Fms-related tyrosine kinase 4 (FLT4) using Cre-Lox technology. After activation with tamoxifen, diphtheria toxin (DT) can be injected into any limb for local ablation. Note the paucity of LYVE-1<sup>+</sup> lymphatic vessels (green) with preservation of CD31<sup>+</sup> blood vessels (red); DAPI staining of nuclei is represented in blue. This model also results in prolonged hindlimb swelling and increased inflammation up to one year post-injection; inflammatory cells are indicated by the brown color.</p></caption><graphic xlink:href="ijms-18-00171-g001"></graphic></fig><fig id="ijms-18-00171-f002" position="float"><label>Figure 2</label><caption><p>Pathophysiologic sequence following CD4<sup>+</sup> cell inflammation in lymphedema. A compromised lymphatic system leads to lymphatic fluid stasis, which subsequently contributes to the accumulation of a distinct CD4<sup>+</sup> inflammatory infiltrate. Although there is a mixed Th1 and Th2 response, Th2 cells in particular have been found to be critical in the development of the pathologic findings of lymphedema. Th2 cytokines IL-4 and IL-13 contribute to lymphedema through the impairment of lymphangiogenesis and upregulation of TGF-β1, which promotes fibrosis. The accumulation of fibrotic components over time ultimately leads to lymphatic dysfunction.</p></caption><graphic xlink:href="ijms-18-00171-g002"></graphic></fig><table-wrap id="ijms-18-00171-t001" position="float"><object-id pub-id-type="pii">ijms-18-00171-t001_Table 1</object-id><label>Table 1</label><caption><p>Summary of selected cytokines and growth factors involved in lymphedema.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Cytokine</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Function</th></tr></thead><tbody><tr><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">IFN-γ</td><td align="center" valign="middle" rowspan="1" colspan="1">Impairs lymphangiogenesis</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Activates macrophages</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">IL-1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Induces DC migration</td></tr><tr><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">IL-13</td><td align="center" valign="middle" rowspan="1" colspan="1">Impairs lymphangiogenesis</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Promotes M2 macrophage activation</td></tr><tr><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">IL-4</td><td align="center" valign="middle" rowspan="1" colspan="1">Impairs lymphangiogenesis</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Promotes M2 macrophage activation</td></tr><tr><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">IL-6</td><td align="center" valign="middle" rowspan="1" colspan="1">Regulates chronic inflammation</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Decreases adipose deposition</td></tr><tr><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">TGF-β1</td><td align="center" valign="middle" rowspan="1" colspan="1">Mediates soft-tissue fibrosis</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Negatively regulates lymphatic vessel regeneration</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">VEGF-C</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Promotes lymphangiogenesis</td></tr></tbody></table></table-wrap></floats-group></pmc><affiliations><list></list><tree><noCountry><name sortKey="Kataru, Raghu P" sort="Kataru, Raghu P" uniqKey="Kataru R" first="Raghu P." last="Kataru">Raghu P. Kataru</name><name sortKey="Ly, Catherine L" sort="Ly, Catherine L" uniqKey="Ly C" first="Catherine L." last="Ly">Catherine L. Ly</name><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J." last="Mehrara">Babak J. Mehrara</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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