Effects of staphylococcal enterotoxin A on the rat gastrointestinal tract

Abstract

Staphylococcal enterotoxin A (SEA) was administered orally (15 jig) to two groups of rats. A marked immune reaction was evoked in the stomach and proximal small intestine of the first group. The second group of rats was used to study the absorptive fate and sites of action of orally administered SEA, utilizing immunoperoxidase staining. After oral dosing of the second group of rats, SEA-related immunoperoxidase staining was confined to: (i) neutrophils and macrophages, principally in the duodenum, and (ii) glomerular neutrophils and cells of the proximal convoluted tubules. Peroxidase staining of the kidney was noted within 15 min of exposure, indicating that SEA or some major postabsorption antigenic product can promptly pass through an intact gastrointestinal mucous membrane and become renally localized. Intestinal and renal detoxification and removal was indicated by an absence of detectable antigen in rats 180 min postexposure. Neuronal binding of SEA in the gastrointestinal tract was not demonstrable.

Superantigen Immune Stimulation Evokes Epithelial Monocyte Chemoattractant Protein 1 and RANTES Production

“…4, and in general accordance with the in vitro findings presented above, small intestinal epithelial cells isolated from SEB-treated mice had a two-to threefold increase in MCP-1 and RANTES mRNAs. These findings add credence to the original postulate that epithelium-derived chemotactic signals might mediate, at least to some degree, the increase in gut T cells observed after systemic SAg treatment (1,3).…”

“…Treatment with the prototypic SAg Staphylococcus aureus enterotoxin B (SEB) was found to result in increased CD3 ϩ T cells in the lamina propria of the mouse jejunum with the cells aligned along the epithelial basement membrane and in an intraepithelial location (1). Likewise, Berry et al have reported increased intraepithelial lymphocytes and lamina propria lymphocytes in the proximal small bowel in SEA-treated rats (3). It has become increasingly apparent that epithelial cells, irrespective of their location, can produce a variety of chemokines (23).…”

Changes in Murine Jejunal Morphology Evoked by the Bacterial SuperantigenStaphylococcus aureusEnterotoxin B Are Mediated by CD4+T Cells

“…In addition to villus-crypt changes, SEB-treated (100 g, 48 h) mice showed increased MHC II expression and an increased number of T cells in the jejunum; many of these cells were in an intraepithelial location or juxtaposed to the epithelial basement membrane. In comparison with this finding, rats treated with S. aureus enterotoxin A showed increased numbers of duodenal intraepithelial lymphocytes 30 to 45 min after treatment (3). The physiological significance of these events remains to be determined, but with the indulgence of speculation, at least two possible consequences can be envisaged.…”

Exotoxins ofStaphylococcus aureus

“…Substance P is one putative mast cell-activating peptide that has been implicated in SEB-induced toxicity (61). However, Beery et al (7) did not detect binding of SEA to nervous tissue in the rat gastrointestinal tract, suggesting that direct induction of neuropeptide release by SEs is unlikely. In conclusion, if the role of mast cells in SFP is confirmed, the mechanisms through which the SEs promote mast cell degranulation remain to be further elucidated.…”