Specific T-cell receptor usage with cytokinemia in Henoch-Schönlein purpura nephritis associated with Staphylococcus aureus infection.
OBJECTIVE
We sought to evaluate the mechanism of Henoch-Schönlein purpura nephritis (HSPN) associated with Staphylococcus aureus (S. aureus) infection.


METHODS
We evaluated six male patients with HSPN associated with S. aureus infection. Routine laboratory examinations, bacteriological examination, histological examination, and analysis of serum cytokine levels were performed in all cases. In addition, peripheral blood mononuclear cells (PBMC) obtained from the six patients and 45 normal individuals were stained with labelled-monoclonal antibodies against six variable parts of the beta-chain (Vbeta) 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 Vbeta-(5.2 + 5.3) and Vbeta 8-positive cells in patients with HSPN were significantly higher than in normal individuals; moreover, specific TCR-Vbeta usage was not observed in patients with HSPN whose S. aureus infection had improved. Serum levels of IL-1beta, 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.


CONCLUSIONS
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.
Hirayama
K
K
Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan. kidney@md.tsukuba.ac.jp
Kobayashi
M
M
Muro
K
K
Yoh
K
K
Yamagata
K
K
Koyama
A
A
D000328:Adult; D016207:Cytokines / Q000097:blood*; D006801:Humans; D011695:IgA Vasculitis / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D007963:Leukocytes, Mononuclear; D008297:Male; D008875:Middle Aged; D009393:Nephritis / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*; D013203:Staphylococcal Infections / Q000150:complications / Q000276:immunology / Q000503:physiopathology*; D013601:T-Lymphocytes / Q000276:immunology
D016207:Cytokines; D016693:Receptors, Antigen, T-Cell, alpha-beta