PMID- 16013011
OWN - NLM
STAT- MEDLINE
DCOM- 20051025
LR  - 20141120
IS  - 1121-8428 (Print)
IS  - 1121-8428 (Linking)
VI  - 18
IP  - 3
DP  - 2005 May-Jun
TI  - Staphylococcal cell membrane antigen, a possible antigen in post-methicillin 
      resistant Staphylococcus aureus (MRSA) infection nephritis and IgA nephropathy, 
      exhibits high immunogenic activity that is enhanced by superantigen.
PG  - 249-56
AB  - 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.
FAU - Shimizu, Yoshio
AU  - Shimizu Y
AD  - Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, 
      Ibaraki, Japan. y-shimz@md.tsukuba.ac.jp
FAU - Sakurai, Hideko
AU  - Sakurai H
FAU - Hirayama, Kouichi
AU  - Hirayama K
FAU - Seki, Masanori
AU  - Seki M
FAU - Yoh, Keigyou
AU  - Yoh K
FAU - Yamagata, Kunihiro
AU  - Yamagata K
FAU - Koyama, Akio
AU  - Koyama A
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - J Nephrol
JT  - Journal of nephrology
JID - 9012268
RN  - 0 (Bacterial Toxins)
RN  - 0 (Cytokines)
RN  - 0 (Enterotoxins)
RN  - 0 (Immunoglobulin A)
RN  - 0 (Immunoglobulin G)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Antigen, T-Cell)
RN  - 0 (Superantigens)
RN  - 0 (enterotoxin F, Staphylococcal)
SB  - IM
MH  - Animals
MH  - Bacterial Toxins/genetics/immunology/metabolism
MH  - Blotting, Western
MH  - Cells, Cultured
MH  - Cytokines/genetics/metabolism
MH  - Disease Models, Animal
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Enterotoxins/genetics/immunology/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Follow-Up Studies
MH  - Glomerulonephritis, IGA/*immunology/microbiology
MH  - Immunoglobulin A/immunology
MH  - Immunoglobulin G/immunology
MH  - In Vitro Techniques
MH  - Methicillin Resistance/*immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Nephritis/*immunology/microbiology
MH  - RNA, Messenger/genetics
MH  - Receptors, Antigen, T-Cell/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Staphylococcus aureus/*immunology
MH  - *Superantigens/genetics/immunology/metabolism
MH  - T-Lymphocytes/immunology/metabolism/pathology
EDAT- 2005/07/14 09:00
MHDA- 2005/10/26 09:00
CRDT- 2005/07/14 09:00
PHST- 2005/07/14 09:00 [pubmed]
PHST- 2005/10/26 09:00 [medline]
PHST- 2005/07/14 09:00 [entrez]
PST - ppublish
SO  - J Nephrol. 2005 May-Jun;18(3):249-56.