Therapeutic lymphangiogenesis ameliorates established acute lung allograft rejection
Identifieur interne : 012908 ( Main/Exploration ); précédent : 012907; suivant : 012909Therapeutic lymphangiogenesis ameliorates established acute lung allograft rejection
Auteurs : Ye Cui [États-Unis] ; Kaifeng Liu [États-Unis] ; Maria E. Monzon-Medina [États-Unis] ; Robert F. Padera ; Hao Wang [États-Unis] ; Gautam George [États-Unis] ; Demet Toprak [États-Unis] ; Elie Abdelnour [États-Unis] ; Emmanuel D Gostino [États-Unis] ; Hilary J. Goldberg [États-Unis] ; Mark A. Perrella [États-Unis] ; Rosanna Malbran Forteza [États-Unis] ; Ivan O. Rosas [États-Unis] ; Gary Visner [États-Unis] ; Souheil El-Chemaly [États-Unis]Source :
- The Journal of Clinical Investigation [ 0021-9738 ] ; ????.
Abstract
Lung transplantation is the only viable option for patients suffering from otherwise incurable end-stage pulmonary diseases such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. Despite aggressive immunosuppression, acute rejection of the lung allograft occurs in over half of transplant recipients, and the factors that promote lung acceptance are poorly understood. The contribution of lymphatic vessels to transplant pathophysiology remains controversial, and data that directly address the exact roles of lymphatic vessels in lung allograft function and survival are limited. Here, we have shown that there is a marked decline in the density of lymphatic vessels, accompanied by accumulation of low-MW hyaluronan (HA) in mouse orthotopic allografts undergoing rejection. We found that stimulation of lymphangiogenesis with VEGF-C156S, a mutant form of VEGF-C with selective VEGFR-3 binding, alleviates an established rejection response and improves clearance of HA from the lung allograft. Longitudinal analysis of transbronchial biopsies from human lung transplant recipients demonstrated an association between resolution of acute lung rejection and decreased HA in the graft tissue. Taken together, these results indicate that lymphatic vessel formation after lung transplantation mediates HA drainage and suggest that treatments to stimulate lymphangiogenesis have promise for improving graft outcomes.
Url:
DOI: 10.1172/JCI79693
PubMed: 26485284
PubMed Central: 4639995
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Lung transplantation is the only viable option for patients suffering from otherwise incurable end-stage pulmonary diseases such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. Despite aggressive immunosuppression, acute rejection of the lung allograft occurs in over half of transplant recipients, and the factors that promote lung acceptance are poorly understood. The contribution of lymphatic vessels to transplant pathophysiology remains controversial, and data that directly address the exact roles of lymphatic vessels in lung allograft function and survival are limited. Here, we have shown that there is a marked decline in the density of lymphatic vessels, accompanied by accumulation of low-MW hyaluronan (HA) in mouse orthotopic allografts undergoing rejection. We found that stimulation of lymphangiogenesis with VEGF-C156S, a mutant form of VEGF-C with selective VEGFR-3 binding, alleviates an established rejection response and improves clearance of HA from the lung allograft. Longitudinal analysis of transbronchial biopsies from human lung transplant recipients demonstrated an association between resolution of acute lung rejection and decreased HA in the graft tissue. Taken together, these results indicate that lymphatic vessel formation after lung transplantation mediates HA drainage and suggest that treatments to stimulate lymphangiogenesis have promise for improving graft outcomes.</p>
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<name sortKey="Abdelnour, Elie" sort="Abdelnour, Elie" uniqKey="Abdelnour E" first="Elie" last="Abdelnour">Elie Abdelnour</name>
<name sortKey="D Gostino, Emmanuel" sort="D Gostino, Emmanuel" uniqKey="D Gostino E" first="Emmanuel" last="D Gostino">Emmanuel D Gostino</name>
<name sortKey="El Chemaly, Souheil" sort="El Chemaly, Souheil" uniqKey="El Chemaly S" first="Souheil" last="El-Chemaly">Souheil El-Chemaly</name>
<name sortKey="Forteza, Rosanna Malbran" sort="Forteza, Rosanna Malbran" uniqKey="Forteza R" first="Rosanna Malbran" last="Forteza">Rosanna Malbran Forteza</name>
<name sortKey="George, Gautam" sort="George, Gautam" uniqKey="George G" first="Gautam" last="George">Gautam George</name>
<name sortKey="Goldberg, Hilary J" sort="Goldberg, Hilary J" uniqKey="Goldberg H" first="Hilary J." last="Goldberg">Hilary J. Goldberg</name>
<name sortKey="Liu, Kaifeng" sort="Liu, Kaifeng" uniqKey="Liu K" first="Kaifeng" last="Liu">Kaifeng Liu</name>
<name sortKey="Monzon Medina, Maria E" sort="Monzon Medina, Maria E" uniqKey="Monzon Medina M" first="Maria E." last="Monzon-Medina">Maria E. Monzon-Medina</name>
<name sortKey="Perrella, Mark A" sort="Perrella, Mark A" uniqKey="Perrella M" first="Mark A." last="Perrella">Mark A. Perrella</name>
<name sortKey="Perrella, Mark A" sort="Perrella, Mark A" uniqKey="Perrella M" first="Mark A." last="Perrella">Mark A. Perrella</name>
<name sortKey="Rosas, Ivan O" sort="Rosas, Ivan O" uniqKey="Rosas I" first="Ivan O." last="Rosas">Ivan O. Rosas</name>
<name sortKey="Toprak, Demet" sort="Toprak, Demet" uniqKey="Toprak D" first="Demet" last="Toprak">Demet Toprak</name>
<name sortKey="Visner, Gary" sort="Visner, Gary" uniqKey="Visner G" first="Gary" last="Visner">Gary Visner</name>
<name sortKey="Wang, Hao" sort="Wang, Hao" uniqKey="Wang H" first="Hao" last="Wang">Hao Wang</name>
</country>
</tree>
</affiliations>
</record>
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