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Review
. 2010 Aug;2(8):2177-97.
doi: 10.3390/toxins2082177. Epub 2010 Aug 18.

Staphylococcal Enterotoxins

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Free PMC article
Review

Staphylococcal Enterotoxins

Irina V Pinchuk et al. Toxins (Basel). .
Free PMC article

Abstract

Staphylococcus aureus (S. aureus) is a Gram positive bacterium that is carried by about one third of the general population and is responsible for common and serious diseases. These diseases include food poisoning and toxic shock syndrome, which are caused by exotoxins produced by S. aureus. Of the more than 20 Staphylococcal enterotoxins, SEA and SEB are the best characterized and are also regarded as superantigens because of their ability to bind to class II MHC molecules on antigen presenting cells and stimulate large populations of T cells that share variable regions on the β chain of the T cell receptor. The result of this massive T cell activation is a cytokine bolus leading to an acute toxic shock. These proteins are highly resistant to denaturation, which allows them to remain intact in contaminated food and trigger disease outbreaks. A recognized problem is the emergence of multi-drug resistant strains of S. aureus and these are a concern in the clinical setting as they are a common cause of antibiotic-associated diarrhea in hospitalized patients. In this review, we provide an overview of the current understanding of these proteins.

Keywords: Staphylococcus aureus; class II MHC; enterotoxins; food-borne poisoning; superantigens.

Figures

Figure 1
Figure 1
Model of the role of mucosal lamina professional and non professional APCs in SE associated Gastro-Intestinal (GI) inflammatory injury. GI inflammatory injury during staphylococcal enterotoxigenic disease is mediated mostly through the SE superantigenic effect on MHC class II expressing mucosal professional (macrophages and dendritic cells, DC) and non professional (such as myofibroblasts) APCs and TCR expressing CD4+ T cells. SE can cross the intestinal epithelial barrier in intact form and bind to class II MHC molecules that expressed on subepithelial myofibroblast. These processes will lead to a strong production of the proinflammatory cytokines and chemokines, including IL-6, IL-8 and MCP-1. The last one may leads to the increased chemotaxis of professional immune cells (CD4+ T cells, Macrophages, DC) from gut associated lymphoid tissue (GALT) to the site of SE associated inflammation in GI mucosa. Those MHC class II:SEs:TCR interactions may in turn result in hyperactivation of the APCs and the T cells leading to the excessive proliferation of T cells and the uncontrolled burst of various proinflammatory cytokines and chemokines causing the superantigen-mediated acute inflammation and shock.
Figure 2
Figure 2
Model of SE interaction with T cell Receptors and class II MHC Molecules. The simultaneous binding of SEs outside of the antigen binding pocket of class II MHC on antigen presenting cells (APC) and to T cell receptors expressing certain Vβ elements allows SEs to act as superantigens. The tripartite interaction of class II MHC:SEs:TcR results in the stimulation of both APC and T cells leading to the production of cytokines by both cell types.

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