CD4(-CELLS MEDIATE SUPERANTIGEN-INDUCED ABNORMALITIES IN MURINE JEJUNAL ION-TRANSPORT() T)

The immunomodulatory properties of bacterial superantigens (SAgs) have been defined, yet comparatively little is known of how SAgs may affec t enteric physiology. Staphylococcus aureus enterotoxin B (SEB) was us ed to examine the ability of SAgs to alter epithelial ion transport. B ALB/c mice, severe combined immunodeficient (SCID, lack T cells) mice, or SCID mice reconstituted with lymphocytes or CD4(+) T cells receive d SEB intraperitoneally, and jejunal segments were examined in Ussing chambers; controls received saline only. Baseline short-circuit curren t (I-sc, indicates net ion transport) and I-sc responses evoked by ele ctrical nerve stimulation, histamine, carbachol, or forskolin were rec orded. Serum levels of interleukin-fl (IL-2) and interferon-gamma (IFN -gamma) were measured. SEB-treated BALB/c mice showed elevated serum I L-2 and IFN-gamma levels, and jejunal segments displayed a time-and do se-dependent increase in baseline I-sc compared with controls. Convers ely, evoked ion secretion was selectively reduced in jejunum from SEB- treated mice. Elevated cytokine levels and changes in jejunal I-sc wer e not observed in SEB-treated SCID mice. In contrast, SCID mice recons tituted with T cells were responsive to SEB challenge as shown by incr eased cytokine production and altered jejunal I-sc responses that were similar to those observed in jejunum from SEB-treated BALB/c mice. We conclude that exposure to a model bacterial SAg causes distinct chang es in epithelial physiology and that these events can be mediated by C D4(+) T cells.