Staphylococcal enterotoxin B increases the severity of type II collagen induced arthritis in mice.
OBJECTIVE
To observe the influence of T cell subset changes on the development of experimental arthritis, by using the bacterial superantigen staphylococcal enterotoxin B (SEB) to modulate the T cell repertoire during the arthritogenic response to type II collagen (CII) in vivo.


METHODS
DBA/1 mice were injected with SEB before immunisation with CII, and assessed for the development of collagen induced arthritis (CIA) and an immune response to CII. Mice with established arthritis were also treated therapeutically with SEB. Flow cytometry was used to evaluate the effect of the therapy on T cell subsets and T cell receptor (TCR) V beta expression.


RESULTS
Mice injected with SEB developed arthritis significantly faster than saline treated control animals, and developed more severe clinical features. Mice treated with SEB after the onset of CIA were also observed to progress more rapidly to a severe arthritis than mice treated with saline alone. The level of anti-CII antibody was not affected by SEB injection. Flow cytometric analysis of TCR expression in mice 21 days after injection of CII showed decreased expression of V beta 6 and V beta 8 cells in SEB treated mice, compared with collagen immunised control mice. Injection of SEB alone caused a decrease in V beta 8, but not V beta 6 T cells compared with the values in normal DBA/1 mice. No significant variations in the T cell repertoire were detected 70 days after CII immunisation.


CONCLUSIONS
Treatment with the bacterial enterotoxin SEB before the induction of arthritis did not suppress the immunological or arthritogenic response to CII in DBA/1 mice, despite the modulation of the V beta 8 T cell subset. Treatment of mice with established arthritis using SEB provoked a more severe disease course.
Wooley
P H
PH
Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA.
Cingel
B
B
D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D001168:Arthritis / Q000276:immunology*; D001323:Autoantibodies / Q000096:biosynthesis; D001327:Autoimmune Diseases / Q000276:immunology*; D003094:Collagen / Q000276:immunology*; D004768:Enterotoxins / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D008198:Lymph Nodes / Q000276:immunology; D051379:Mice; D008811:Mice, Inbred DBA; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000032:analysis; D013211:Staphylococcus aureus / Q000276:immunology; D018089:Superantigens / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology; D013997:Time Factors
D000942:Antigens, Bacterial; D001323:Autoantibodies; D004768:Enterotoxins; D016693:Receptors, Antigen, T-Cell, alpha-beta; D018089:Superantigens; C031818:enterotoxin B, staphylococcal; D003094:Collagen