The effect of selenium on the autophagy of macrophage infected by Staphylococcus aureus

Area of Science:

• Immunology and Microbiology
• Cellular Biology
• Nutritional Science

Background:

• Staphylococcus aureus (S. aureus) infection triggers inflammatory responses in macrophages.
• The role of selenium in modulating autophagy during S. aureus infection remains unclear.
• Macrophages play a critical role in innate immunity against bacterial pathogens.

Purpose of the Study:

• To investigate the effect of selenium on autophagy in RAW264.7 macrophages infected with S. aureus.
• To elucidate the impact of selenium on the MAPK and NF-κB inflammatory signaling pathways.
• To determine selenium's influence on S. aureus proliferation within macrophages.

Main Methods:

• RAW264.7 macrophages were co-treated with sodium selenite (Na2SeO3) and S. aureus.
• Western blotting was used to assess autophagy-related proteins (LC3, p62) and signaling pathway components (MAPK, NF-κB).
• Immunofluorescence staining quantified microtubule-binding protein light chain 3 (LC3) puncta, transmission electron microscopy (TEM) examined cellular ultrastructure, and plate counting measured bacterial proliferation.

Main Results:

• Selenium supplementation increased LC3-II expression and decreased p62 levels, indicating enhanced autophagy.
• Increased intracellular LC3 puncta, autophagic vesicles, autophagosomes, and autolysosomes were observed with selenium treatment.
• Selenium significantly inhibited the phosphorylation of key proteins in the MAPK and NF-κB signaling pathways.
• Bacterial proliferation of S. aureus within macrophages was reduced by selenium.

Conclusions:

• Selenium promotes autophagy and alleviates autophagic flux blockade in S. aureus-infected macrophages.
• Selenium suppresses the MAPK and NF-κB signaling pathways, reducing inflammation.
• Selenium effectively inhibits S. aureus proliferation in macrophages, suggesting a therapeutic potential.