Korean J Intern Med.  1998 Feb;13(1):27-32.

Role of mononuclear cells of IgA nephropathy on ICAM-1 expression in mesangial cells

• Lee TW
• Park JK
• Ahn JH
• Ihm CG
• Kim MJ

Abstract

OBJECTIVES
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. METHODS: 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-alpha, IL-1 beta and culture supernants of PBMC were analyzed using a cell ELISA method. The concentration of IL-1 beta and TNF-alpha in culture supernatants was measured by using a commercially available radioimmunoassay kit. RESULTS: Addition of human recombinant TNF-alpha induced an increased ICAM-1 expression in a dose-dependent manner. The expression of ICAM-1 was further increased after co-stimulation with TNF-alpha and IL-1 beta. 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-alpha and IL-1 beta in supernatants from the patients with IgA nephropathy was significantly higher than that from those with non-IgA nephropathy. CONCLUSION: TNF-alpha 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.

MeSH Terms

Animal
Cells, Cultured
Glomerular Mesangium/immunology
Glomerular Mesangium/cytology
Glomerulonephritis, IGA/immunology*
Glomerulonephritis, IGA/etiology
Human
Intercellular Adhesion Molecule-1/metabolism*
Interleukin-1/secretion
Interleukin-1/pharmacology
Leukocytes, Mononuclear/immunology
Mice
Tumor Necrosis Factor/secretion
Tumor Necrosis Factor/pharmacology