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1
*
Department of Microbiology and Immunology, University of Adelaide, North Terrace, Adelaide, South Australia, Australia; and
Centre de Recherche en Rhumatologie et Immunologie, Centre de Recherche du Centre Hospitalier de l’Université Laval (CHUL), Ste-Foy, Quebec, Canada;
Pfizer Central Research, Groton, CT 06340; and
§
Biomedical Research Center, University of British Columbia, Vancouver, British Columbia, Canada
Superantigens such as staphylococcal enterotoxin A and B (SEA and
SEB) activate the immune system by stimulating a large proportion of T
lymphocytes through specific Vß regions of the TCR and activating
macrophages by binding to MHC class II molecules. While the mechanisms
by which superantigens activate T lymphocytes have been elucidated,
their role in the generation of local immune responses to bacterial
invasion is still unclear. In this study we have examined the ability
of the superantigens SEA and SEB to elicit an inflammatory reaction in
vivo, in s.c. air pouches in the mouse. Upon injection into the s.c.
air pouch, the two superantigens stimulated a time-dependent increase
in the number of leukocytes appearing in the pouch exudate. The
leukocytes migrating into the pouch exudate were predominantly
neutrophils, with some mononuclear phagocytes and eosinophils present.
No T lymphocytes were detected either in the pouch lining tissue or in
the exudate cells. Injection of SEA resulted in increased ICAM-1
expression, as detected by immunohistochemistry, on endothelial cells
in the tissue surrounding the air pouch and accumulation of TNF-
and
the chemokines macrophage inflammatory protein-2 (MIP-2), MIP-1, and
JE in the pouch exudate. In addition, pretreatment of mice with
Abs raised against ICAM-1, TNF-, MIP-2, MIP-1, KC, or
JE inhibited leukocyte accumulation induced by SEA. These data
demonstrate that bacterial superantigens may promote inflammation at
extravascular sites in vivo, and that this response is secondary to the
generation of inflammatory mediators, including
chemokines.
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