STUDIES ON THE INTERACTION BETWEEN GP-180-DEFICIENT NEUTROPHILS AND VASCULAR ENDOTHELIUM

  • 1 January 1982
    • journal article
    • research article
    • Vol. 60  (1) , 160-165
Abstract
A patient whose neutrophils lacked the glycoprotein gp-180 showed an increased susceptibility to bacterial infections. Neutrophils from this patient migrated abnormally in vivo and in vitro. To examine the basis for this abnormality in migration, the interaction of gp-180-deficient neutrophils with artificial surfaces and with human endothelial cell cultures was studied. Compared with normal neutrophils, gp-180-deficient neutrophils showed decreased adhesion to cold-insoluble globulin-coated plastic surfaces and their ability to spread on this substratum was greatly impaired. Gp-180-deficient neutrophils interacted in a normal fashion with endothelial monolayers, attaching to their upper surfaces and migrating between cell junctions to spread between the monolayers and the subjacent plastic. A normal interaction with endothelium in vivo was implied by the finding that the rise in the neutrophil count in response to epinephrine, an index of the marginated pool, was normal in the gp-180-deficient patient. The abnormal function of gp-180-deficient cells is unlikely to be caused by a faulty interaction with the vascular endothelium. These cells migrate poorly in vivo because of an abnormal interaction with extravascular connective tissue matrix constituents.