Abstract
Staphylococcal enterotoxin B (SEB) and related superantigenic toxins are potent stimulators of the immune system and cause a variety of diseases in humans, ranging from food poisoning to toxic shock. These toxins bind directly to major histocompatibility complex (MHC) class II molecules on antigen-presenting cells and specific Vβ regions of T-cell receptors (TCR), resulting in hyperactivation of both monocytes/macrophages and T lymphocytes. Activated host cells produce massive amounts of proinflammatory cytokines and chemokines, activating inflammation and coagulation, causing clinical symptoms that include fever, hypotension, and shock. This review summarizes the in vitro and in vivo effects of staphylococcal superantigens, the role of pivotal mediators induced by these toxins in the pathogenic mechanisms of tissue injury, and the therapeutic agents to mitigate the toxic effects of superantigens.
Highlights
Staphylococcal enterotoxin B (SEB) and related superantigenic toxins are potent stimulators of the immune system and cause a variety of diseases in humans, ranging from food poisoning to toxic shock
Staphylococcus aureus, a ubiquitous gram-positive coccus, produces several exotoxins: staphylococcal enterotoxins A through R (SEA-SER), and toxic shock syndrome toxin 1 (TSST-1), which contribute to its ability to cause disease in humans and laboratory animals [1,2,3,4,5,6,7,8]
Superantigens in the SEA subfamily can bind to both and chains of major histocompatibility complex (MHC) class II, interacting with the OB fold and -grasp domain, respectively. This mode of superantigen and MHC class II interaction enables the toxin to bind to both sides of the molecule and cross-link MHC class II on antigen-presenting cells (APC) [40]
Summary
Staphylococcus aureus, a ubiquitous gram-positive coccus, produces several exotoxins: staphylococcal enterotoxins A through R (SEA-SER), and toxic shock syndrome toxin 1 (TSST-1), which contribute to its ability to cause disease in humans and laboratory animals [1,2,3,4,5,6,7,8]. The chemokines, IL-8, monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein 1α (MIP-1α), and MIP-1 , are induced directly by SEB or TSST-1 and selectively activate and direct migration of leukocytes, neutrophils and dendritic cells to sites of tissue injury [16,17]. These mediators are pathogenic at high concentrations in vivo and induce fever, organ dysfunction, and death
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