Role of Mononuclear Cells of IgA Nephropathy on ICAM - 1 Expression in Mesangial Cells

Abstract

To investigate the possible role of mononuclear cells and their products in the pathogenesis of IgA nephropathy, in vitro expression of ICAM-1 on cultured mouse mesangial cell(MC) was examined after stimulation with mononuclear cell culture supernatant from patients with IgA nephropathy. Peripheral blood mononuclear cells (PBMC) were isolated and cultured from 18 patients with primary IgA nephropathy, 8 normal controls and 5 patients with non-IgA nephropathy (FSGS 1, MGN 3, MPGN 1). ICAM-1 expression on cultured mouse MC by TNF-α, IL-1β and culture supernants of PBMC were analyzed using a cell ELISA method. The concentration of IL-1β and TNF-α in culture supernatants was measured by using a commercially available radioimmunoassay kit. Addition of human recombinant TNF-α induced an increased ICAM-1 expression in a dose-dependent manner. The expression of ICAM-1 was further increased after co-stimulation with TNF-α and IL-1β. Addition of PBMC culture supernatants into mouse MC induced significantly higher expression of ICAM-1 by supernatants from the patients with IgA nephropathy compared with that from normal controls. The concentration of TNF-α and IL-1β in supernatants from the patients with IgA nephropathy was significantly higher than that from those with non-IgA nephropathy. TNF-α and IL-1 released from mononuclear cells induced the up-regulation of ICAM-1 expression and this may be related to the immune pathogenesis of IgA nephropathy.