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

Biol Trace Elem Res. 2022 Feb;200(2):761-767. doi: 10.1007/s12011-021-02676-4. Epub 2021 Mar 23.

Abstract

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.

Keywords: NLRP3; S. aureus; Selenium; TLR2.

MeSH terms

  • Animals
  • Inflammasomes*
  • Inflammation
  • Interleukin-1beta
  • Macrophages
  • Mice
  • NLR Family, Pyrin Domain-Containing 3 Protein*
  • RAW 264.7 Cells
  • Selenium* / pharmacology
  • Signal Transduction*
  • Staphylococcus aureus
  • Toll-Like Receptor 2*

Substances

  • Inflammasomes
  • Interleukin-1beta
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Nlrp3 protein, mouse
  • Tlr2 protein, mouse
  • Toll-Like Receptor 2
  • Selenium