Human endothelial cell damage induced by interactions between polymorphonuclear leukocytes and immune complex-coated erythrocytes.

We have examined, in vitro, the effects of autologous erythrocytes (RBC) coated with soluble immune complexes (RBC-IC) on the interactions of polymorphonuclear leukocytes (PMN) with human endothelial cell (EC) cultures. RBC-IC were prepared by incubating human RBC with soluble immune complexes, prepared with keyhole limpet hemocyanin (KLH) and rabbit anti-KLH in antigen excess, using normal human serum as a complement source. Several parameters believed to be related to EC-PMN interactions, including adherence of PMN to EC, detachment of EC after incubation with media harvested from RBC-IC-stimulated PMN, and the release of 2-deoxy-D-[3H]glucose from damaged EC, were investigated. The proportion of PMN adhering to EC increased in direct proportion to the number of RBC-IC used to stimulate PMN. Media harvested from PMN stimulated with RBC, RBC incubated with complement, RBC-IC, or opsonized zymosan caused variable degrees of detachment of cultured EC. The percentage of EC detached was directly related to the intensity of the PMN degranulation as measured by lysozyme release with a correlation coefficient of 0.935, comparing the natural log of the lysozyme released to the percentage EC detachment. Finally, RBC-IC added to PMN and EC induced PMN-mediated EC damage as measured by the release of 2-deoxy-D-[3H]glucose from the labeled EC. The release of 2-deoxy-D-[3H]glucose from the labeled EC was directly related to the number of RBC-IC used to stimulate the PMN. These data indicate that RBC-IC are able to stimulate the type of interactions between PMN and EC that are believed to cause EC damage and may play a role in the initiation or exacerbation of inflammatory vascular lesions.