MiR-124-3p/EIF3B Regulates Host Cell Apoptosis Induced by Chlamydia psittaci Through PI3K/AKT Signaling Pathway

Area of Science:

• Microbiology
• Cell Biology
• Molecular Biology

Background:

• Chlamydia psittaci is a zoonotic pathogen causing human respiratory illness.
• Chlamydia infections are linked to apoptosis, with microRNAs (miRNAs) mediating regulatory roles.

Purpose of the Study:

• To investigate the role of miR-124-3p in C. psittaci-induced apoptosis in human bronchial epithelial (HBE) cells.
• To elucidate the regulatory mechanism involving miR-124-3p, its target gene EIF3B, and the PI3K/AKT signaling pathway.

Main Methods:

• Infection of HBE cells with C. psittaci.
• Analysis of apoptosis, miRNA and mRNA expression levels.
• Luciferase reporter assays to confirm target gene interaction.
• Inhibitor/mimic transfection and siRNA knockdown experiments.
• Western blotting to assess protein expression and pathway activation.

Main Results:

• C. psittaci infection induced significant HBE cell apoptosis and upregulated miR-124-3p.
• EIF3B was identified as a direct target of miR-124-3p, with inverse expression correlation.
• Inhibition of miR-124-3p decreased apoptosis and C. psittaci replication while inhibiting PI3K/AKT.
• miR-124-3p mimic showed opposite effects, and EIF3B siRNA reversed miR-124-3p inhibitor effects.

Conclusions:

• miR-124-3p promotes apoptosis in C. psittaci-infected HBE cells by targeting EIF3B.
• The PI3K/AKT signaling pathway is activated by this miR-124-3p/EIF3B axis.
• This study reveals a novel molecular mechanism in Chlamydia-host cell interactions.