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

Ting Tong1,2, Yunfei Li1, You Zhou1

  • 1Department of public health laboratory sciences, school of public health, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.

The Journal of Infectious Diseases
|November 19, 2024
PubMed

Insights

Chlamydia psittaci infection triggers apoptosis in human bronchial epithelial cells via miR-124-3p targeting EIF3B. This mechanism activates the PI3K/AKT pathway, influencing disease progression.

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.
Keywords:
Chlamydia psittaciEIF3BPI3K/AKT signaling pathwayapoptosismiR-124-3p

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