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• W2580141069 abstract "Abstract Staphylococcal superantigens cause toxic shock syndrome, which is characterized by massive T cell activation and a predominant Th1 profile of cytokine production. However, superantigen-producing Staphylococcus aureus strains are often part of the human nasal microbiome, and this carrier state has often been associated with some type 2 immune responses such as chronic sinusitis with polyps and atopic dermatitis. We have previously reported that the S. aureus cell wall downregulates the human T cell response to superantigens through a TLR2-dependent, IL-10–mediated mechanism. In this study, we show that S. aureus also regulates the profile of superantigen-induced T cell recruitment. The staphylococcal superantigen SEE induced the production of Th1 cell–recruiting chemokines, including IP-10, through an IFN-γ–dependent mechanism. Such an induction was suppressed by the concomitant presence of S. aureus. The downregulation of IP-10 by S. aureus was mediated by components of its cell wall, but was not due to peptidoglycan-induced IL-10 production. Instead, S. aureus triggered activation of MAPKs p38 and ERK, as well as inhibition of STAT1 signaling in monocytes, altogether contributing to the downregulation of IP-10 and other Th1 cell–recruiting chemokines (e.g., CXCL9 and CXCL11). These effects translated into inhibition of superantigen-induced Th1 cell recruitment. Taken together, our data may explain why colonization of superantigen-producing S. aureus can induce, under some circumstances, mucosal type 2 immune responses." @default.
• W2580141069 created "2017-02-03" @default.
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• W2580141069 date "2017-03-01" @default.
• W2580141069 modified "2023-10-18" @default.
• W2580141069 title "<i>Staphylococcus aureus</i> Downregulates IP-10 Production and Prevents Th1 Cell Recruitment" @default.
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• W2580141069 doi "https://doi.org/10.4049/jimmunol.1601336" @default.
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