Cytokines and T-cell responses in superantigen-related glomerulonephritis following methicillin-resistant Staphylococcus aureus infection

Background. We have previously reported that 10 patients who developed glom erulonephritis (GN) in association with methicillin-resistant Staphylococcu s aureus (MRSA) infection showed a marked increase in DR + CD4+ and DR + CD 8+ subsets of T cells and in T cells expressing several T-cell receptor (TC R) V beta + cells, perhaps representing VP-specific T-cell activation by MR SA-derived superantigens (Kidney Int 1995; 47: 207-216). In this study we e xamine cytokine levels, T-lymphocyte subsets, natural killer NK cells, memo ry T cells, and the expression of IL-2 receptors in order to better underst and the role of bacterial superantigens and cytokines in the pathogenesis o f MRSA-associated GN. Methods. Twenty-two patients with MRSA infection who later developed GN cau sed by staphylococcal enterotoxin were evaluated immunologically in compari son with patients whose MRSA infection was not followed by GN (non-GN group ) and normal individuals. Results. Among peripheral lymphocytes, the frequency of T cells expressing several TCR V beta s, especially V beta 5-family TCR, was higher in the GN group than in both the non-GN group and the normal healthy control group. G N patients also showed increased serum levels of several cytokines, includi ng tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) , IL-2, IL-6, IL-8, and IL-10, which have been implicated in the onset of n ephritis. Memory cells, and IL-2 receptors also were elevated in the GN gro up. Conclusion. These results suggest that T cells activated by MRSA-derived st aphylococcal enterotoxins and subsequent production of cytokines may play a n important role in the pathogenesis of MRSA-associated GN.