Regulation of inflammation and fibrosis by macrophages in lymphedema
Identifieur interne : 001901 ( Main/Exploration ); précédent : 001900; suivant : 001902Regulation of inflammation and fibrosis by macrophages in lymphedema
Auteurs : Swapna Ghanta [États-Unis] ; Daniel A. Cuzzone [États-Unis] ; Jeremy S. Torrisi [États-Unis] ; Nicholas J. Albano [États-Unis] ; Walter J. Joseph [États-Unis] ; Ira L. Savetsky [États-Unis] ; Jason C. Gardenier [États-Unis] ; David Chang [États-Unis] ; Jamie C. Zampell [États-Unis] ; Babak J. Mehrara [États-Unis]Source :
- American Journal of Physiology - Heart and Circulatory Physiology [ 0363-6135 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Biopsie, Chimiotaxie des leucocytes, Différenciation cellulaire, Facteur de croissance endothéliale vasculaire de type C (métabolisme), Facteurs temps, Femelle, Fibrose, Humains, Inflammation (anatomopathologie), Inflammation (immunologie), Inflammation (métabolisme), Inflammation (physiopathologie), Irradiation corporelle totale, Lymphocytes auxiliaires Th2 (immunologie), Lymphocytes auxiliaires Th2 (métabolisme), Lymphoedème (anatomopathologie), Lymphoedème (immunologie), Lymphoedème (métabolisme), Lymphoedème (physiopathologie), Macrophages (immunologie), Macrophages (métabolisme), Modèles animaux de maladie humaine, Phénotype, Souris de lignée C57BL, Transplantation de moelle osseuse, Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (immunologie), Vaisseaux lymphatiques (métabolisme), Vaisseaux lymphatiques (physiopathologie), Études cas-témoins.
- MESH :
- anatomopathologie : Inflammation, Lymphoedème, Vaisseaux lymphatiques.
- immunologie : Inflammation, Lymphocytes auxiliaires Th2, Lymphoedème, Macrophages, Vaisseaux lymphatiques.
- métabolisme : Facteur de croissance endothéliale vasculaire de type C, Inflammation, Lymphocytes auxiliaires Th2, Lymphoedème, Macrophages, Vaisseaux lymphatiques.
- physiopathologie : Inflammation, Lymphoedème, Vaisseaux lymphatiques.
- Animaux, Biopsie, Chimiotaxie des leucocytes, Différenciation cellulaire, Facteurs temps, Femelle, Fibrose, Humains, Irradiation corporelle totale, Modèles animaux de maladie humaine, Phénotype, Souris de lignée C57BL, Transplantation de moelle osseuse, Études cas-témoins.
English descriptors
- KwdEn :
- Animals, Biopsy, Bone Marrow Transplantation, Case-Control Studies, Cell Differentiation, Chemotaxis, Leukocyte, Disease Models, Animal, Female, Fibrosis, Humans, Inflammation (immunology), Inflammation (metabolism), Inflammation (pathology), Inflammation (physiopathology), Lymphatic Vessels (immunology), Lymphatic Vessels (metabolism), Lymphatic Vessels (pathology), Lymphatic Vessels (physiopathology), Lymphedema (immunology), Lymphedema (metabolism), Lymphedema (pathology), Lymphedema (physiopathology), Macrophages (immunology), Macrophages (metabolism), Mice, Inbred C57BL, Phenotype, Th2 Cells (immunology), Th2 Cells (metabolism), Time Factors, Vascular Endothelial Growth Factor C (metabolism), Whole-Body Irradiation.
- MESH :
- chemical , metabolism : Vascular Endothelial Growth Factor C.
- immunology : Inflammation, Lymphatic Vessels, Lymphedema, Macrophages, Th2 Cells.
- metabolism : Inflammation, Lymphatic Vessels, Lymphedema, Macrophages, Th2 Cells.
- pathology : Inflammation, Lymphatic Vessels, Lymphedema.
- physiopathology : Inflammation, Lymphatic Vessels, Lymphedema.
- Animals, Biopsy, Bone Marrow Transplantation, Case-Control Studies, Cell Differentiation, Chemotaxis, Leukocyte, Disease Models, Animal, Female, Fibrosis, Humans, Mice, Inbred C57BL, Phenotype, Time Factors, Whole-Body Irradiation.
Abstract
Lymphedema, a common complication of cancer treatment, is characterized by inflammation, fibrosis, and adipose deposition. We have previously shown that macrophage infiltration is increased in mouse models of lymphedema. Because macrophages are regulators of lymphangiogenesis and fibrosis, this study aimed to determine the role of these cells in lymphedema using depletion experiments. Matched biopsy specimens of normal and lymphedema tissues were obtained from patients with unilateral upper extremity breast cancer-related lymphedema, and macrophage accumulation was assessed using immunohistochemistry. In addition, we used a mouse tail model of lymphedema to quantify macrophage accumulation and analyze outcomes of conditional macrophage depletion. Histological analysis of clinical lymphedema biopsies revealed significantly increased macrophage infiltration. Similarly, in the mouse tail model, lymphatic injury increased the number of macrophages and favored M2 differentiation. Chronic macrophage depletion using lethally irradiated wild-type mice reconstituted with CD11b-diphtheria toxin receptor mouse bone marrow did not decrease swelling, adipose deposition, or overall inflammation. Macrophage depletion after lymphedema had become established significantly increased fibrosis and accumulation of CD4+ cells and promoted Th2 differentiation while decreasing lymphatic transport capacity and VEGF-C expression. Our findings suggest that macrophages home to lymphedematous tissues and differentiate into the M2 phenotype. In addition, our findings suggest that macrophages have an antifibrotic role in lymphedema and either directly or indirectly regulate CD4+ cell accumulation and Th2 differentiation. Finally, our findings suggest that lymphedema-associated macrophages are a major source of VEGF-C and that impaired macrophage responses after lymphatic injury result in decreased lymphatic function.
Url:
DOI: 10.1152/ajpheart.00598.2014
PubMed: 25724493
PubMed Central: 4551121
Affiliations:
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Cuzzone</name><affiliation wicri:level="2"><nlm:aff id="aff1">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York</wicri:cityArea></affiliation></author><author><name sortKey="Torrisi, Jeremy S" sort="Torrisi, Jeremy S" uniqKey="Torrisi J" first="Jeremy S." last="Torrisi">Jeremy S. Torrisi</name><affiliation wicri:level="2"><nlm:aff id="aff1">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York</wicri:cityArea></affiliation></author><author><name sortKey="Albano, Nicholas J" sort="Albano, Nicholas J" uniqKey="Albano N" first="Nicholas J." last="Albano">Nicholas J. Albano</name><affiliation wicri:level="2"><nlm:aff id="aff1">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York</wicri:cityArea></affiliation></author><author><name sortKey="Joseph, Walter J" sort="Joseph, Walter J" uniqKey="Joseph W" first="Walter J." last="Joseph">Walter J. Joseph</name><affiliation wicri:level="2"><nlm:aff id="aff1">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York</wicri:cityArea></affiliation></author><author><name sortKey="Savetsky, Ira L" sort="Savetsky, Ira L" uniqKey="Savetsky I" first="Ira L." last="Savetsky">Ira L. Savetsky</name><affiliation wicri:level="2"><nlm:aff id="aff1">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York</wicri:cityArea></affiliation></author><author><name sortKey="Gardenier, Jason C" sort="Gardenier, Jason C" uniqKey="Gardenier J" first="Jason C." last="Gardenier">Jason C. Gardenier</name><affiliation wicri:level="2"><nlm:aff id="aff1">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York</wicri:cityArea></affiliation></author><author><name sortKey="Chang, David" sort="Chang, David" uniqKey="Chang D" first="David" last="Chang">David Chang</name><affiliation wicri:level="2"><nlm:aff id="aff2">The Department of Surgery, Division of Plastic and Reconstructive Surgery, University of Chicago Medical Center, Chicago, Illinois</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Illinois</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, University of Chicago Medical Center, Chicago</wicri:cityArea></affiliation></author><author><name sortKey="Zampell, Jamie C" sort="Zampell, Jamie C" uniqKey="Zampell J" first="Jamie C." last="Zampell">Jamie C. Zampell</name><affiliation wicri:level="2"><nlm:aff id="aff1">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York</wicri:cityArea></affiliation></author><author><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J." last="Mehrara">Babak J. Mehrara</name><affiliation wicri:level="2"><nlm:aff id="aff1">The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, New York;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York</wicri:cityArea></affiliation></author></analytic><series><title level="j">American Journal of Physiology - Heart and Circulatory Physiology</title><idno type="ISSN">0363-6135</idno><idno type="eISSN">1522-1539</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biopsy</term><term>Bone Marrow Transplantation</term><term>Case-Control Studies</term><term>Cell Differentiation</term><term>Chemotaxis, Leukocyte</term><term>Disease Models, Animal</term><term>Female</term><term>Fibrosis</term><term>Humans</term><term>Inflammation (immunology)</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Inflammation (physiopathology)</term><term>Lymphatic Vessels (immunology)</term><term>Lymphatic Vessels (metabolism)</term><term>Lymphatic Vessels (pathology)</term><term>Lymphatic Vessels (physiopathology)</term><term>Lymphedema (immunology)</term><term>Lymphedema (metabolism)</term><term>Lymphedema (pathology)</term><term>Lymphedema (physiopathology)</term><term>Macrophages (immunology)</term><term>Macrophages (metabolism)</term><term>Mice, Inbred C57BL</term><term>Phenotype</term><term>Th2 Cells (immunology)</term><term>Th2 Cells (metabolism)</term><term>Time Factors</term><term>Vascular Endothelial Growth Factor C (metabolism)</term><term>Whole-Body Irradiation</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Biopsie</term><term>Chimiotaxie des leucocytes</term><term>Différenciation cellulaire</term><term>Facteur de croissance endothéliale vasculaire de type C (métabolisme)</term><term>Facteurs temps</term><term>Femelle</term><term>Fibrose</term><term>Humains</term><term>Inflammation (anatomopathologie)</term><term>Inflammation (immunologie)</term><term>Inflammation (métabolisme)</term><term>Inflammation (physiopathologie)</term><term>Irradiation corporelle totale</term><term>Lymphocytes auxiliaires Th2 (immunologie)</term><term>Lymphocytes auxiliaires Th2 (métabolisme)</term><term>Lymphoedème (anatomopathologie)</term><term>Lymphoedème (immunologie)</term><term>Lymphoedème (métabolisme)</term><term>Lymphoedème (physiopathologie)</term><term>Macrophages (immunologie)</term><term>Macrophages (métabolisme)</term><term>Modèles animaux de maladie humaine</term><term>Phénotype</term><term>Souris de lignée C57BL</term><term>Transplantation de moelle osseuse</term><term>Vaisseaux lymphatiques (anatomopathologie)</term><term>Vaisseaux lymphatiques (immunologie)</term><term>Vaisseaux lymphatiques (métabolisme)</term><term>Vaisseaux lymphatiques (physiopathologie)</term><term>Études cas-témoins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Vascular Endothelial Growth Factor C</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Inflammation</term><term>Lymphoedème</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Inflammation</term><term>Lymphocytes auxiliaires Th2</term><term>Lymphoedème</term><term>Macrophages</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Inflammation</term><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Macrophages</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Inflammation</term><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Macrophages</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Inflammation</term><term>Lymphocytes auxiliaires Th2</term><term>Lymphoedème</term><term>Macrophages</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Lymphatic Vessels</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Inflammation</term><term>Lymphoedème</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Inflammation</term><term>Lymphatic Vessels</term><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Biopsy</term><term>Bone Marrow Transplantation</term><term>Case-Control Studies</term><term>Cell Differentiation</term><term>Chemotaxis, Leukocyte</term><term>Disease Models, Animal</term><term>Female</term><term>Fibrosis</term><term>Humans</term><term>Mice, Inbred C57BL</term><term>Phenotype</term><term>Time Factors</term><term>Whole-Body Irradiation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Biopsie</term><term>Chimiotaxie des leucocytes</term><term>Différenciation cellulaire</term><term>Facteurs temps</term><term>Femelle</term><term>Fibrose</term><term>Humains</term><term>Irradiation corporelle totale</term><term>Modèles animaux de maladie humaine</term><term>Phénotype</term><term>Souris de lignée C57BL</term><term>Transplantation de moelle osseuse</term><term>Études cas-témoins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Lymphedema, a common complication of cancer treatment, is characterized by inflammation, fibrosis, and adipose deposition. We have previously shown that macrophage infiltration is increased in mouse models of lymphedema. Because macrophages are regulators of lymphangiogenesis and fibrosis, this study aimed to determine the role of these cells in lymphedema using depletion experiments. Matched biopsy specimens of normal and lymphedema tissues were obtained from patients with unilateral upper extremity breast cancer-related lymphedema, and macrophage accumulation was assessed using immunohistochemistry. In addition, we used a mouse tail model of lymphedema to quantify macrophage accumulation and analyze outcomes of conditional macrophage depletion. Histological analysis of clinical lymphedema biopsies revealed significantly increased macrophage infiltration. Similarly, in the mouse tail model, lymphatic injury increased the number of macrophages and favored M2 differentiation. Chronic macrophage depletion using lethally irradiated wild-type mice reconstituted with CD11b-diphtheria toxin receptor mouse bone marrow did not decrease swelling, adipose deposition, or overall inflammation. Macrophage depletion after lymphedema had become established significantly increased fibrosis and accumulation of CD4<sup>+</sup> cells and promoted Th2 differentiation while decreasing lymphatic transport capacity and VEGF-C expression. Our findings suggest that macrophages home to lymphedematous tissues and differentiate into the M2 phenotype. In addition, our findings suggest that macrophages have an antifibrotic role in lymphedema and either directly or indirectly regulate CD4<sup>+</sup> cell accumulation and Th2 differentiation. Finally, our findings suggest that lymphedema-associated macrophages are a major source of VEGF-C and that impaired macrophage responses after lymphatic injury result in decreased lymphatic function.</p></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Illinois</li><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Ghanta, Swapna" sort="Ghanta, Swapna" uniqKey="Ghanta S" first="Swapna" last="Ghanta">Swapna Ghanta</name></region><name sortKey="Albano, Nicholas J" sort="Albano, Nicholas J" uniqKey="Albano N" first="Nicholas J." last="Albano">Nicholas J. Albano</name><name sortKey="Chang, David" sort="Chang, David" uniqKey="Chang D" first="David" last="Chang">David Chang</name><name sortKey="Cuzzone, Daniel A" sort="Cuzzone, Daniel A" uniqKey="Cuzzone D" first="Daniel A." last="Cuzzone">Daniel A. Cuzzone</name><name sortKey="Gardenier, Jason C" sort="Gardenier, Jason C" uniqKey="Gardenier J" first="Jason C." last="Gardenier">Jason C. Gardenier</name><name sortKey="Joseph, Walter J" sort="Joseph, Walter J" uniqKey="Joseph W" first="Walter J." last="Joseph">Walter J. Joseph</name><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J." last="Mehrara">Babak J. Mehrara</name><name sortKey="Savetsky, Ira L" sort="Savetsky, Ira L" uniqKey="Savetsky I" first="Ira L." last="Savetsky">Ira L. Savetsky</name><name sortKey="Torrisi, Jeremy S" sort="Torrisi, Jeremy S" uniqKey="Torrisi J" first="Jeremy S." last="Torrisi">Jeremy S. Torrisi</name><name sortKey="Zampell, Jamie C" sort="Zampell, Jamie C" uniqKey="Zampell J" first="Jamie C." last="Zampell">Jamie C. Zampell</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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