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

Chlamydia psittaci is a zoonotic pathogen known to cause respiratory diseases in humans. Chlamydia infections are closely associated with apoptosis, in which microRNAs (miRNAs) play regulatory roles. Herein, we demonstrated that C. psittaci infection induces apoptosis in human bronchial epithelial (HBE) cells and investigated regulatory mechanism involving miR-124-3p and the PI3K/AKT signaling pathway. Following C. psittaci infection in HBE cells, we observed an elevated HBE cell apoptosis, accompanied by upregulation of miR-124-3p levels. Mechanistically, we identified EIF3B as a novel target gene of miR-124-3p, supported by the inverse correlation of their mRNA expressions. MiR-124-3p inhibitor reduced apoptosis induced by C. psittaci, increased the replication of C. psittaci, and inhibited PI3K/AKT activation, whereas miR-124-3p mimic produced opposite effects, and transfection with EIF3B siRNA reversed the effects of miR-124-3p inhibitor. Our findings suggest that miR-124-3p targeting EIF3B promotes apoptosis in C. psittaci-infected HBE cells through activation of the PI3K/AKT signaling pathway. C. psittaci infection increased HBE cells apoptosis, accompanied by upregulation of miR-124-3p levels and downregulation of EIF3B levels. MiR-124-3p targeting EIF3B promotes apoptosis in C. psittaci-infected HBE cells through the activation of the PI3K/AKT signaling pathway.