Modulation of cytokine production from an EpiOcular corneal cell culture model in response to Staphylococcus aureus superantigen

Abstract

The present study investigated the hypothesis that Staphylococcus aureus enterotoxin B (SEB) produces epithelial cell death and releases inflammatory cytokines that produce stromal infiltration during contact lens induced peripheral ulceration. Epithelial cells were incubated with different doses of SEB for various time periods. Culture supernatants were assayed for cytokines IL-1 beta, IL-6 and chemotactic agents IL-8 and LTB4 SEB induced the production of IL-1 beta and IL-8. Epithelial cells exposed for longer periods (48 h) with low concentrations of SEB produced significantly higher levels (P < 0.02) of IL-1 beta and IL-8 (P < 0.05) compared to a 24 h exposure. SEB did not induce the production of IL-6 and LTB4.

Staphylococcus aureus enterotoxin B, protein A, and lipoteichoic acid stimulations in nasal polyps

“…21 Furthermore, SEB induced IL-12p40 production in peritoneal mice macrophages, 22 and a culture of corneal epithelial cells has been shown to release IL-8 after treatment with SEB. 23 In this study, neither IL-12p70 nor IL-8 was upregulated after SEB stimulation in inferior turbinates and NP. However, similar ex vivo studies are required because results of animal studies cannot necessarily be projected onto human beings.…”

Staphylococcus aureus superantigens and airway disease

“…Epithelial cells have also been shown to release proinflammatory cytokines, including IL-1β and IL-8, following treatment with SEB [35]. Co-culture of epithelial cells with T cells also leads to indirect superantigen-mediated effects on epithelial cell activity and function, as a result of epithelial accessory cell function for superantigen-induced T-cell activation.…”

“…Co-culture of epithelial cells with T cells also leads to indirect superantigen-mediated effects on epithelial cell activity and function, as a result of epithelial accessory cell function for superantigen-induced T-cell activation. Possibly, the most notable and important effects of this interaction are on epithelial ion transport and barrier functions, which are adversely affected by SEB and thought to be due to increased release of IFNγ and TNFα from the T cells [35,36]. It has been demonstrated that these adverse epithelial effects may be attenuated by nitric oxide, IL-10 and TGFβ2 [35,37].…”

Gram‐positive bacterial superantigen outside‐in signaling causes toxic shock syndrome

“…SEB induced increased IL‐5, IL‐6, IL‐8 and granulocyte macrophage colony‐stimulating factor responses from human nasal epithelial cells [88–90]. SEB also elicited increased IL‐1β and IL‐8 from corneal epithelial cells [91].…”