Studies on the pathogenesis of glomerulonephritis and vascultitis induced by superantigen.

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Background. We have previously reported that 10 patients who developed glomerulonephritis (GN) in association with methicillin-resistant staphylococcus aureus (MRSA) infection showed a marked increase in T cells both in DR+CD4+ and DR+CD8+ subsets and in T cells expressing several T cell receptor (TCR) Vb+ cells, perhaps representing Vb-specific T cell activation by MRSA-derived superantigens (Kidney Int 1995 ; 47 : 207-2 16). Moreover, we tested levels of cytokines, T-lymphocy te subsets, natural killer NK cells, memory T cells, and the expression of IL-2 receptors in order to better understand the role of bacterial superantigens and cytokines in the pathogenesis of MRSA- associated GN.Methods. Twenty-two patients with MRSA infection who later developed glomerulonephritis (GN) caused by staphylococcal enterotoxin were evaluated immunologically in comparison with patients whose MRSA infection was not followed by GN (non-GN group) and normal individuals.Results. Among peripheral lymphocytes, frequency of T cells expressing several TCR Vb's, especially Vb5-family TCR was higher in GN group than in the non-GN group as well as in normal healthy control. GN patients also showed increased serum levels of several cytokines, including tumor necrosis factor-a, interleukin-1b (IL-1b), IL-2, IL-6, IL-8, and IL-l0, which have been suggested to be responsible for the onset of nephritis. Memory cells, and IL-2 receptors also were elevated in GN group than in normal individuals.Conclusion, These results suggest that T cells activated by MRSA-derived staphylococcal enterotoxins and subsequent production of cytokines may play important roles in the pathogenesis of MRSA-associated GN.