Fig. 4: DCA inhibits S. aureus-induced NF-κB and NLRP3 activation by activating TGR5 in MMECs. | npj Biofilms and Microbiomes

Fig. 4: DCA inhibits S. aureus-induced NF-κB and NLRP3 activation by activating TGR5 in MMECs.

From: Gut microbiota-mediated secondary bile acid alleviates Staphylococcus aureus-induced mastitis through the TGR5-cAMP-PKA-NF-κB/NLRP3 pathways in mice

Fig. 4: DCA inhibits S. aureus-induced NF-κB and NLRP3 activation by activating TGR5 in MMECs.

A–G Cells were pretreated with DCA (10, 20, and 30 μM) for 2 h followed by S. aureus treatment for the next 24 h and the protein levels of the NF-κB and NLRP3 pathways from the indicated groups were determined by western blotting (A). The relative intensities of p-p65, p-IκB, NLRP3, ASC, and IL-1β were determined (B–G). H–N Cells were pretreated with SBI-115 for 2 h and then treated with DCA (30 μM) for an additional 2 h followed by S. aureus treatment for the next 24 h. The protein levels of the NF-κB and NLRP3 pathways were determined by western blotting (H), and the relative intensities of p-p65, p-IκB, NLRP3, ASC, and IL-1β were determined (I–N). O–U. Cells were pretreated with siRNA-TGR5 or siRNA-neg for 48 h followed by DCA (30 μM) and S. aureus treatment as mentioned above, and the protein levels of the NF-κB and NLRP3 pathways were determined by western blotting. Data are expressed as the means ± SD (B–G, I–N, and P–U) and one-way ANOVA was performed, followed by Tukey’s test (B–G, I–N, and P–U). *p < 0.05, **p < 0.01, ***p < 0.001 indicate significance. ns, no significance.

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