BACKGROUND
The post-methicillin resistant Staphlylococcus aureus (MRSA) infection nephritis is a progressive glomerulonephritis that occurs following Staphylococcus aureus infection. It has been assumed that staphylococcal superantigens and other cellular antigens are necessary for the development of post-MRSA infection nephritis, and we have previously identified a staphylococcal cell membrane antigen (GenBank, accession number; BAB41819.1) as a possible antigen in post-MRSA infection nephritis. In this study, we assessed the immunogenic activity of the staphylococcal cell membrane antigen and determined the relationship between the cell membrane antigen and superantigen.
METHODS
Balb/c mice were immunized with glutathione S-transferase (GST) or staphylococcal cell membrane antigen-GST fusion protein. One week later, their lymphocytes were cultured with or without toxic shock syndrome toxic-1 (TSST-1) for one week. Immunoglobulin levels in the culture supernatants were measured by ELISA, and transcript expressions for cytokines, and the T-cell receptors (TCR) Vbeta17 (activated by TSST-1), Vbeta1 and Vbeta8 (not activated by TSST-1) in the culture were analyzed by reverse transcriptase polymerase chain reaction.
RESULTS
Neither IgG nor IgA were detected in the culture supernatant of GST-primed lymphocytes, with or without TSST-1. In contrast, IgG and IgA levels gradually increased in direct proportion to the TSST-1 concentration in the supernatants of staphylococcal cell membrane antigen-GST fusion protein-primed lymphocytes. Various cytokine messenger RNA (mRNA) transcripts were detected in both GST-primed and staphylococcal cell membrane antigen-GST-primed cells in the presence of TSST-1. A Vbeta17 transcript could not be detected during the early culture phase under both culture conditions, while Vbeta1 and Vbeta8 T-cells survived for 7 days in the staphylococcal cell membrane antigen-GST fusion protein-primed culture in the presence of TSST-1.
CONCLUSION
These results suggest that staphylococcal cell membrane antigen-GST-primed T-cells were stimulated more than GST-primed cells. Their activity was enhanced further in the presence of cytokines, which were induced by TSST-1, such that the T-cells were able to survive and activate B-cells to produce immunoglobulins.