This study aimed to investigate the effects of selenium (Se) on the expression of Toll-like receptor (TLR) 2 and pyrin domain-containing protein (NLRP)3 inflammasome in macrophages infected by Staphylococcus aureus (S. aureus). RAW 264.7 macrophages were treated with 2 μmol/L Na2SeO3 for 12 h before infection with S. aureus for 2 h. Through Western blot, qRT-PCR, and ELISA analysis, the core molecules of TLR2 signaling pathway and NLRP3 inflammasome in RAW 264.7 macrophages were detected. Results showed that Se significantly reduced the elevated mRNA expression of TLR2, myeloid differentiation factor-88 (Myd88), NLRP3, Caspase-recruitment domain (ASC), and Caspase-1 induced by S. aureus. Furthermore, compared with I group, the protein expression of TLR2, Myd88, NLRP3, ASC, and Caspase-1 were suppressed in T group. In addition, the mRNA and protein expression of interleukin-1 beta (IL-1β) induced by S. aureus were also decreased after Se treatment. In conclusion, Se inhibits S. aureus-induced inflammation by suppressing the activation of the TLR2 signaling pathway and NLRP3 inflammasome in RAW 264.7 macrophages.

This study aimed to investigate the effects of dietary selenium during pregnancy on the selenium deposition and antioxidant enzymes in postpartum mouse serum, liver, and mammary gland. Eighty BALB/c pregnant mice were randomly divided into four groups: CG (Se-deficient basal diet, n = 20), LG (0.05 mg/kg Se-supplemented diet, n = 20), MG (0.1 mg/kg Se-supplemented diet, n = 20), and HG (0.2 mg/kg Se-supplemented diet, n = 20). Four days after parturition, all mice were euthanized. The selenium deposition and antioxidants enzymes in serum, liver, and mammary gland were detected. Results show that with increasing selenium supplementation, the selenium deposition and activation of T-AOC, T-SOD, and GSH-Px increased, meanwhile the concentration of MDA decreased in serum, liver, and mammary gland. Therefore, this study suggested selenium was mainly deposited in the liver, and dietary selenium during pregnancy might improve the antioxidant status in postpartum animals.

Background Some research has indicated that selenium (Se) plays a significant role during mastitis. However the intracellular anti-inflammatory effect of Se is not fully clear. Due to the ability of Staphylococcus aureus ( S. aureus ) to internalize into host cell, in this study we explored whether Se could regulate inflammation induced by S. aureus through reactive oxygen species (ROS)-mediated NLRP3 inflammasome in bMECs. Result bMECs were treated with 8 μmol/L Na 2 SeO 3 for 12 h before infected with S. aureus for 2 h. Through flow cytometry, Western blot and qPCR analysis, ROS and NLRP3 imflammasome were detected. Result shown that the production of ROS was increased by S. aureus , Se exerted strong inhibitory effects on the production of ROS; The protein expression of NLRP3 inflammasome including NLRP3, ASC and Caspase-1 increased significantly after S. aureus infection, Se played an important role in regulating the expression of NLRP3, ASC and Caspase-1; To further investigate the anti-inflammatory effect of Se, the expression level of IL-1β associated molecule pro-IL-1β and IL-1β were detected. Result shown that the mRNA expression of IL-1β was up-regulated by S. aureus and after Se treatment the expression level of IL-1β mRNA was markedly down-regulated, meanwhile Se play a regulation effect on the protein expression of Pro-IL-1β and IL-1β. Conclusions Here we show that ROS is involved in bMECs inflammation induced by S. aureus and Se ameliorates S. aureus -induced inflammation through ROS-mediated NLRP3 pathway in bMECs.

Selenium is an essential micronutrient that plays an important role in immunity. However, the mechanism that Selenium modulates mastitis is not fully clear. In this experiment, we investigated whether selenium can inhibit the activation of the NLRP3 inflammasome in a mouse model of Staphylococcus aureus-induced mastitis. Eighty BALB/c female mice were fed with experimental Selenium deficiency basal diet for 2 weeks to achieve the purpose of selenium consumption until pregnancy. Pregnant mice were randomly divided into four groups (control group; selenium supplement group; Staphylococcus aureus infection group and Staphylococcus aureus infection after selenium supplement group). Twenty-four hours after challenging, all mice were euthanized and mammary tissue samples were aseptically collected. Through pathological staining, western blot analysis, real-time fluorescence quantitative polymerase chain reaction analysis, and enzyme-linked immunosorbent assay, the regulation effect of Selenium on NLRP3 inflammasome was detected. The result showed that compared with the control group, selenium significantly inhibited the expression of NLRP3, ASC, Caspase-1, Caspase-1 p20, and Pro-IL-1β (p < 0.01). Meanwhile the mRNA expression and release of IL-1β was suppressed in the treatment group compared with Staphylococcus aureus infection group (p < 0.01). Therefore, these results suggest that dietary selenium can attenuate Staphylococcus aureus mastitis by inhibition of the NLRP3 inflammasome.