MiR-124-3p/EIF3B regulates host cell apoptosis induced by Chlamydia psittaci through PI3K/AKT signaling pathway.

Abstract

Chlamydia psittaci is a zoonotic pathogen known to cause respiratory diseases in humans. Chlamydia infections are closely associated with apoptosis, in which 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 of HBE cells 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 inhibitors reduced apoptosis induced by C. psittaci, increased the replication of C. psittaci and inhibited the PI3K/AKT activated, whereas miR-124-3p mimics produced opposite effects, and transfection with EIF3B siRNA reversed the effects of miR-124-3p inhibitors. Our findings suggest that miR-124-3p targeting EIF3B promotes apoptosis in C. psittaci-infected HBE cells through the activation of PI3K/AKT signaling pathway.