Enterococcus faecalis lipoteichoic acid regulates macrophages autophagy via PI3K/Akt/mTOR pathway

Area of Science:

• Immunology
• Microbiology
• Cell Biology

Background:

• Enterococcus faecalis (E. faecalis) is a key factor in persistent apical periodontitis (PAP).
• The precise mechanisms by which E. faecalis interacts with immune cell autophagy remain unclear.
• Understanding these interactions is crucial for developing targeted therapies for PAP.

Purpose of the Study:

• To investigate the role of E. faecalis lipoteichoic acid (LTA) in macrophage autophagy.
• To elucidate the signaling pathways involved in E. faecalis-induced autophagy in macrophages.
• To determine the dependence of this process on Beclin1.

Main Methods:

• Macrophage cell cultures were treated with purified E. faecalis LTA.
• Autophagy activation was assessed by monitoring autophagosome formation and autophagy-related protein levels.
• Expression of key signaling proteins, including p-Akt and p-mTOR, was analyzed.
• Experiments were conducted in the presence and absence of Beclin1 knockdown in macrophages.

Main Results:

• E. faecalis LTA significantly activated macrophage autophagy, evidenced by increased autophagosomes and autophagy-related proteins.
• Treatment with E. faecalis LTA led to a significant decrease in the expression of phosphorylated Akt (p-Akt) and phosphorylated mTOR (p-mTOR).
• The observed activation of autophagy and downregulation of p-Akt/p-mTOR by E. faecalis LTA was abolished in macrophages with Beclin1 knockdown.

Conclusions:

• E. faecalis LTA promotes macrophage autophagy.
• This autophagy induction is mediated by the inhibition of the PI3K/Akt/mTOR signaling pathway.
• The Beclin1 protein is essential for E. faecalis LTA-induced macrophage autophagy.