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

Ting Tong; Yunfei Li; You Zhou; Xindian Zeng; Cui Xiao; Saihong Cao; Chuan Wang; Zhongyu Li; Zhou Zhou; Qinqin Bai; Shenghua Chen; Shuwu Yan; Lili Chen

doi:10.1093/infdis/jiae573

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

J Infect Dis. 2024 Nov 19:jiae573. doi: 10.1093/infdis/jiae573. Online ahead of print.

Authors

Ting Tong^{1

2}, Yunfei Li¹, You Zhou¹, Xindian Zeng³, Cui Xiao¹, Saihong Cao¹, Chuan Wang⁴, Zhongyu Li⁴, Zhou Zhou⁴, Qinqin Bai¹, Shenghua Chen⁴, Shuwu Yan⁵, Lili Chen¹

Affiliations

¹ Department of public health laboratory sciences, school of public health, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
² Liangping center for disease control and prevention, Liangping, Chongqing, 405200, China.
³ Department of medical record, Affliated Nanhua Hospital, University of South China, Hengyang 421002, Hunan Province, China.
⁴ School of Basic Medicine, Hengyang medical school, University of South China, Hengyang, Hunan, China.
⁵ Hengyang center for disease control and prevention, Hengyang, Hunan, 421001, China.

PMID: 39561162
DOI: 10.1093/infdis/jiae573

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.

Keywords: Chlamydia psittaci; EIF3B; PI3K/AKT signaling pathway; apoptosis; miR-124-3p.

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