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ANTIINFLDEL

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Cerrado

The anti inflammatory actions of Developmental Endothelial Locus 1 Del 1

Leukocyte recruitment is an important component of inflammatory and autoimmune disorders and consists of selectin-mediated rolling, the chemokine-induced activation of leukocytes, the integrin-dependent firm adhesion and the subse... ver más

31/08/2014

TUD

100K€

Presupuesto del proyecto: 100K€

Líder del proyecto

TECHNISCHE UNIVERSITAET DRESDEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2014-08-31 No tenemos la información de la convocatoria

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No hay información privada compartida para este proyecto. Habla con el coordinador.

1 Participantes

TUD

0.00€ | Lider

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Líder del proyecto

TECHNISCHE UNIVERSITAET DRESDEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 100K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Leukocyte recruitment is an important component of inflammatory and autoimmune disorders and consists of selectin-mediated rolling, the chemokine-induced activation of leukocytes, the integrin-dependent firm adhesion and the subsequent transendothelial migration. LFA-1 is an important leukocyte integrin mediating adhesion by binding to its endothelial counter-receptors ICAM-1 and -2. Whereas many adhesion receptors are known to promote leukocyte recruitment, very little information exists about endogenous inhibitors of the cascade. The lab of the applicant has recently identified the endothelial-derived secreted molecule Developmental Endothelial Locus-1 (Del-1, Edil3) as a potent endogenous inhibitor of the leukocyte adhesion cascade. Del-1 acted as an inhibitor of LFA-1-dependent leukocyte adhesion to the endothelium. Consistently, Del-1-/- mice displayed a pro-inflammatory phenotype with higher leukocyte recruitment in vivo. Recently, we found that Del-1 expression is abundant in the immunoprivileged eye. In the first aim of the present project we plan to study the expression and functional contribution of Del-1 in models of eye inflammation. These studies may identify Del-1 as novel therapeutic approach in eye inflammation. In addition, previous reports have demonstrated that Del-1 is elevated by tissue ischemia or hypoxia. Relative tissue hypoxia is a hallmark of acute inflammation. The mechanisms regulating the hypoxia-related anti-inflammatory response are not well understood. In the second aim of this project we will study whether Del-1 acts to regulate the hypoxia-related anti-inflammatory response. The pro-inflammatory effects of hypoxia in mice can be tested in models of ambient hypoxic exposure (e.g. 8% oxygen for 4-8 h) that induce increased permeability of endothelial and epithelial barriers e.g. lung and intestine, as well as enhanced recruitment of inflammatory cells. In summary the present proposal will focus on characterizing further the fun

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