期刊
JOURNAL OF INTERNAL MEDICINE
卷 249, 期 4, 页码 289-295出版社
WILEY
DOI: 10.1046/j.1365-2796.2001.00815.x
关键词
cytokine; Henoch-Schonlein purpura nephritis; Staphylococcus aureus; T-cell receptor
Objectives, We sought to evaluate the mechanism of Henoch-Schonlein purpura nephritis (HSPN) associated with Staphylococcus aureus (S. aureus) infection. Design, We evaluated six male patients with HSPN associated with S. aureus infection. Routine laboratory examinations, bacteriological examination, histological examination, and analysis of serum levels were performed in all cases. In peripheral blood mononuclear cells obtained from the six patients and 45 normal individuals were stained with labelled-monoclonal antibodies against six variable parts of the beta -chain (V beta) of the T-cell receptor (TCR), and stained cells were analysed by flow cytometry. Results, Patients with HSPN associated with S. aureus infection showed features of the nephrotic syndrome with rapidly progressive glomerulonephritis. as well as varying degrees of mesangial proliferative glomerulonephritis with crescent formation, Serological examination showed elevated levels of serum IgA and IgG as well as immune complexes after the onset of infection. The percentage of V beta-(5.2 + 5.3) and V beta 8-positive cells in patients with HSPN were significantly higher than in normal individuals; moreover, specific TCR-V beta usage was not observed in patients with HSPN whose S. aureus infection had improved. Serum levels of IL-1 beta, IL-2, IL-6, IL-8 and TNF-alpha in patients with HSPN were significantly higher than in normal individuals, and normalized at the healing stage of S. aureus infection. Conclusion, Conventional antigens and/or staphylococcal enterotoxins originated from S. aureus might have been involved in the pathogenesis of HSPN in the present cohort. Therefore, steroid or other immunosuppressive therapies could not be utilized despite the high activity of glomerulonephritis, and as a result the prognoses of these cases of HSPN were serious.
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