Abstract
Staphylococcal enterotoxin B (SEB) and related exotoxins are important virulence factors produced by Staphylococcus aureus as they cause human diseases such as food poisoning and toxic shock. These toxins bind directly to cells of the immune system resulting in hyperactivation of both T lymphocytes and monocytes/macrophages. The excessive release of proinflammatory cytokines from these cells mediates the toxic effects of SEB. This study examined the inhibitory activities of an anti-inflammatory drug, sulfasalazine, on SEB-stimulated human peripheral blood mononuclear cells (PBMC). Sulfasalazine dose-dependently inhibited tumor necrosis factor α, interleukin 1 (IL-1) β, IL-2, IL-6, interferon γ (IFNγ), and various chemotactic cytokines from SEB-stimulated human PBMC. Sulfasalazine also potently blocked SEB-induced T cell proliferation and NFκB activation. These results suggest that sulfasalazine might be useful in mitigating the toxic effects of SEB by blocking SEB-induced host inflammatory cascade and signaling pathways.
Highlights
Staphylococcal enterotoxin B (SEB) and structurally related bacterial exotoxins are etiological agents that cause a variety of diseases in humans, ranging from food poisoning, autoimmune diseases, and toxic shock [1,2,3]
SFZ has immune-modulatory effects including inhibition of cyclooxygenase- and lipoxygenase-dependent pathways, enhancing anti-inflammatory adenosine release from sites of inflammation, and reducing leukocyte adhesion to endothelial cells [17,18]. This brief report presents the inhibitory activities of SFZ on SEB-activated human peripheral blood mononuclear cells (PBMC)
The potency of SFZ in blocking cytokines and chemokines in SEB-stimulated human PBMC was investigated since proinflammatory mediators play key roles in superantigen-induced toxic shock
Summary
Staphylococcal enterotoxin B (SEB) and structurally related bacterial exotoxins are etiological agents that cause a variety of diseases in humans, ranging from food poisoning, autoimmune diseases, and toxic shock [1,2,3] These exotoxins potently stimulate host immune responses by binding directly to the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells and specific Vβ regions of the T-cell receptors [4,5]. SFZ has immune-modulatory effects including inhibition of cyclooxygenase- and lipoxygenase-dependent pathways, enhancing anti-inflammatory adenosine release from sites of inflammation, and reducing leukocyte adhesion to endothelial cells [17,18]. This brief report presents the inhibitory activities of SFZ on SEB-activated human peripheral blood mononuclear cells (PBMC)
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