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

Area of Science:

• Immunology
• Microbiology
• Nutritional Science

Background:

• Staphylococcus aureus (S. aureus) infection triggers inflammatory responses in macrophages.
• Toll-like receptor 2 (TLR2) and NLRP3 inflammasome are critical mediators of this inflammatory response.
• Selenium (Se) is an essential trace element with known immunomodulatory properties.

Purpose of the Study:

• To investigate the effect of selenium (Se) on the expression of TLR2 and NLRP3 inflammasome components.
• To determine if Se can modulate the inflammatory response of macrophages infected with S. aureus.

Main Methods:

• RAW 264.7 macrophages were treated with sodium selenite (Na2SeO3) and subsequently infected with S. aureus.
• Quantitative real-time PCR (qRT-PCR) and Western blot were used to detect mRNA and protein expression levels.
• Enzyme-linked immunosorbent assay (ELISA) was employed to measure cytokine levels.

Main Results:

• Se treatment significantly reduced the S. aureus-induced mRNA expression of TLR2, Myd88, NLRP3, ASC, and Caspase-1.
• Protein levels of TLR2, Myd88, NLRP3, ASC, and Caspase-1 were also suppressed by Se.
• Se significantly decreased the mRNA and protein expression of interleukin-1 beta (IL-1β).

Conclusions:

• Selenium (Se) effectively inhibits S. aureus-induced inflammation in macrophages.
• Se exerts its anti-inflammatory effect by suppressing the activation of the TLR2 signaling pathway and NLRP3 inflammasome.
• These findings highlight the potential of selenium in managing S. aureus infections.