Staphylococcal enterotoxins in the etiopathogenesis of mucosal autoimmunity within the gastrointestinal tract

Abstract

The staphylococcal enterotoxins (SEs) are the products of Staphylococcus aureus and are recognized as the causative agents of classical food poisoning in humans following the consumption of contaminated food. While illness evoked by ingestion of the SE or its producer organism in tainted food are often self-limited, our current understanding regarding the evolution of S. aureus provokes the utmost concern. The organism and its associated toxins, has been implicated in a wide variety of disease states including infections of the skin, heart, sinuses, inflammatory gastrointestinal disease, toxic shock, and Sudden Infant Death Syndrome. The intricate relationship between the various subsets of immunocompetent T cells and accessory cells and the ingested material found within the gastrointestinal tract present daunting challenges to the maintenance of immunologic homeostasis. Dysregulation of the intricate balances within this environment has the potential for extreme consequences within the host, some of which are long-lived. The focus of this review is to evaluate the relevance of staphylococcal enterotoxin in the context of mucosal immunity, and the underlying mechanisms that contribute to the pathogenesis of gastrointestinal autoimmune disease.

Figure 1

Staphylococcal enterotoxin B (SEB) induces apoptosis in mouse Spleen. (A) Normal splenic tissue from a 12 week-old C57BL/10J mouse as seen in 10× magnification and 20× (B); Representative Peyer’s patch tissue excised from a 12 week-old C57BL/10J mouse gavaged with SEB is shown in 20× magnifcation (C) and 40× (D). Tissues were excised 6 days following oral treatment. Immunohistochemical TUNEL staining of the tissues was performed where darkly stained cells are indicative of apoptosis. Note the darkly-stained apoptotic cells in the expanded follicular area of the SEB-treated spleen section. Staining was performed using a Trevigen TACS^R TdT In Situ Apoptosis Detection Kit.

Figure 2

Staphylococcal enterotoxin B (SEB) induces apoptosis in mouse Peyer’s patches. (A) Normal Peyer’s patch tissue from a 12 week-old C57BL/10J mouse demonstrating germinal center containing lymphocytes; (B) Representative Peyer’s patch tissue excised from a 12 week-old C57BL/10J mouse gavaged with SEB. Tissues were excised 6 days following oral treatment. Immunohistochemical TUNEL staining of the tissues was performed where darkly stained cells are indicative of apoptosis. Note the darkly-stained apoptotic cells in the expanded follicular area of the SEB-treated Peyer’s patch section. Staining was performed using a Trevigen TACS^R TdT In Situ Apoptosis Detection Kit.