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Del-1, an endogenous leukocyte-endothelial adhesion inhibitor, limits inflammatory cell recruitment.

Science (New York, N.Y.) | Nov 14, 2008

http://www.ncbi.nlm.nih.gov/pubmed/19008446

Leukocyte recruitment to sites of infection or inflammation requires multiple adhesive events. Although numerous players promoting leukocyte-endothelial interactions have been characterized, functionally important endogenous inhibitors of leukocyte adhesion have not been identified. Here we describe the endothelially derived secreted molecule Del-1 (developmental endothelial locus-1) as an anti-adhesive factor that interferes with the integrin LFA-1-dependent leukocyte-endothelial adhesion. Endothelial Del-1 deficiency increased LFA-1-dependent leukocyte adhesion in vitro and in vivo. Del-1-/- mice displayed significantly higher neutrophil accumulation in lipopolysaccharide-induced lung inflammation in vivo, which was reversed in Del-1/LFA-1 double-deficient mice. Thus, Del-1 is an endogenous inhibitor of inflammatory cell recruitment and could provide a basis for targeting leukocyte-endothelial interactions in disease.

Pubmed ID: 19008446 RIS Download

Mesh terms: Animals | Bronchoalveolar Lavage Fluid | Carrier Proteins | Cell Adhesion | Endothelial Cells | Intercellular Adhesion Molecule-1 | Leukocyte Rolling | Ligands | Lipopolysaccharides | Lung | Lymphocyte Function-Associated Antigen-1 | Mice | Monocytes | Neutrophil Infiltration | Neutrophils | Peritonitis | Pneumonia | Recombinant Fusion Proteins

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Associated grants

  • Agency: NIAID NIH HHS, Id: AI067254
  • Agency: NHLBI NIH HHS, Id: R01 HL082927
  • Agency: Intramural NIH HHS, Id: Z01 BC010790-01

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