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Abstract
Type I interferon (IFN) induction is a critical component of innate immune response to viral and bacterial infection, including S. aureus, but whether it activates the signaling in macrophages and the regulation mechanisms is less well understood. Here we show that S. aureus infection promoted the IFN-β mRNA expression and stimulator of IFN genes (STING)/TANK-binding kinase 1 (TBK1)/interferon regulatory factor 3 (IRF3)-dependent production of IFN-β. Infection with S. aureus induced caspase recruitment domain and membrane-associated guanylate kinase-like domain protein 3 (CARMA3) expression at both the mRNA and protein levels. The heat-killed bacteria failed to trigger IRF3 phosphorylation and upregulation of CARMA3 expression. However, overexpression of CARMA3 did not affect phosphorylation of TBK1 or IRF3 in RAW264.7 cells, J774A.1 macrophages, and mouse embryonic fibroblast (MEF) cells. In conclusion, S. aureus infection induces STING/TBK1/IRF3-mediated IFN-β production in a CARMA3-independent manner.
Highlights
We explored the effect of exthat S. aureus infection increased lactate dehydrogenase (LDH) release from 6 to 24 hpi (Figure 2G)
Upon infection at a MOI of 200, the transcriptional the stimulator of IFN genes (STING)/TANK-binding kinase 1 (TBK1)/interferon regulatory factor 3 (IRF3) pathway, we first sought to determine the mRNA and protein levlevels were elevated at 1 hpi, and continued to be increased at 12 hpi
Many reports have demonstrated that S. aureus can persist intracellularly [7,16], and utilizes the intracellular environment as a critical refuge for survival and dissemination in the hosts via manipulation of innate immunity, including autophagy [17] and apoptosis [18]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. S. aureus infection induc duction of type I IFNs in lymphocytes and airway epithelial cells [8], and higher levels of IFN-β in dendritic cells (DCs) [9,10]. Aureus infection induces thetic double-stranded RNA (dsRNA) analog poly(I:C) in MEFs [11]. In this stu production of type I IFNs in lymphocytes and airway epithelial cells [8], and higher mRNA found that S. aureus infection triggers activation of the STING/TBK1/IRF3 pathw levels of IFN-β in dendritic cells (DCs) [9,10]. To test the ability of S. aureus to induce IFN-β signaling in macrophages, we different time points and at various multi of infection. IFN-β mRNA expression and IFN-β production in RAW264.7 cells. production in RAW264.7
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