Selenium Attenuates S. aureus-Induced Inflammation by Regulation TLR2 Signaling Pathway and NLRP3 Inflammasome in RAW 264.7 Macrophages.

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-1ß) 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.

Selenium Plays an Anti-Inflammatory Role by Regulation NLRP3 Inflammasome in Staphylococcus aureus-Infected Mouse Mammary Gland.

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-1ß (p < 0.01). Meanwhile the mRNA expression and release of IL-1ß 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.

Short Communication: Effects of Dietary Selenium Supplementation on Selenium Deposition and Antioxidant Status in Postpartum Mice.

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.

Selenium inhibits Staphylococcus aureus-induced inflammation by suppressing the activation of the NF-κB and MAPK signalling pathways in RAW264.7 macrophages.

Inflammation is the hallmark of Staphylococcus aureus (S. aureus)-induced mastitis. Given the interesting relationship between selenium levels and inflammation, this study aimed to demonstrate that selenium modulated the inflammation reaction by suppressing the nuclear factor kappa B (NF-κB) and mitogen activated protein kinase (MAPK) signalling pathways. RAW264.7 macrophages were treated with three different concentrations (1µmol/l, 1.5µmol/l, and 2µmol/l) of Na2SeO3 for 12h before infection with S. aureus for 6h, 8h, and 10h. The results showed that selenium significantly reduced the mRNA expression levels of tumour necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1ß), and interleukin-6 (IL-6). Furthermore, the release of TNF-α, IL-1ß, and IL-6 was decreased significantly with selenium supplementation. In addition, selenium influenced the NF-κB signalling pathway by suppressing the activation of NF-κB p65 and degradation of inhibitory kappa-B (IκB). Selenium also suppressed extracellular regulated protein kinase (Erk), c-Jun N-terminal kinase (Jnk), and p38 phosphorylation through the MAPK signalling pathway. In conclusion, selenium played an anti-inflammation role in RAW264.7 macrophages infected with S. aureus by suppressing the activation of the NF-κB and MAPK signalling pathways.