Role of mononuclear cells of IgA nephropathy on ICAM-1 expression in mesangial cells.
- Author:
Tae Won LEE
1
;
Jai Kyung PARK
;
Jae Hyung AHN
;
Chun Gyoo IHM
;
Myung Jae KIM
Author Information
1. Department of Internal Medicine, College of Medicine, Kyunghee University, Seoul, Korea.
- Publication Type:Original Article
- MeSH:
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
- From:The Korean Journal of Internal Medicine
1998;13(1):27-32
- CountryRepublic of Korea
- Language:English
-
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.
