Expression and correlation analysis of IL-4, IFN-γ and FcαRI in tonsillar mononuclear cells in patients with IgA nephropathy

Background: Clinical deterioration of IgA nephropathy (IgAN) is frequently preceded by episodes of upper respiratory tract infection such as tonsillitis. The aim of this study was attempt to investigate the expression and correlation of IL-4, IFN-gamma and Fc alpha RI in tonsillar mononuclear cells under stimulations of a-hemolytic streptococcus (HS) or lipopolysaccharide (LPS) in patients with IgA nephropathy. Methods: Tonsillar mononuclear cells isolated from 26 patients with IgAN and 25 patients with chronic tonsillitis (CT) as controls were cultured for 72 h with or without a-hemolytic streptococcus (HS) and lipopolysaccharide (LPS) stimulation. Concentration of IL-4 and IFN-gamma level were determined by ELISA. Expression levels of IL-4, IFN-gamma and Fc alpha RI mRNA were measured by real-time PCR, respectively. FcaRI expressing cells were tracked by flow cytometry. Results: The supernatant concentration of IL-4, IFN-gamma and the expression of IL-4, IFN-gamma and FcaRI mRNA in the IgA nephropathy group was markedly increased compared with the non-IgAN group. With the stimulation of HS, the production of IL-4 and the FcaRI expressing cells in the IgA nephropathy group was significantly increased than the non-IgAN group, while the secretion of IFN-gamma was remarkably decreased in the IgA nephropathy group than the non-IgAN group. Upon the LPS stimulation, the concentration of IL-4, IFN-gamma in the supernatant of the IgA nephropathy group was markedly increased compared with the non-IgAN group. However, there wasn't significant difference in the Fc alpha RI expressing cells between the LPS stimulated IgAN group and the non-IgAN group. The expression of FcaRI is in a negative correlation with IL-4 while positive with IFN-gamma. Conclusion: The tonsillar mononuclear cells of IgAN may in a state of overactive immune response, which probably can promote the secretion of Th cytokines, involving in the pathogenesis of IgAN. (C) 2014 Elsevier Inc. All rights reserved.