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.

中文翻译：

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MiR-124-3p/EIF3B 通过 PI3K/AKT 信号通路调节鹦鹉热衣原体诱导的宿主细胞凋亡


鹦鹉热衣原体是一种人畜共患病原体，已知可引起人类呼吸系统疾病。衣原体感染与细胞凋亡密切相关，其中 miRNA 起调节作用。在此，我们证明了鹦鹉热衣原体感染诱导人支气管上皮 （HBE） 细胞凋亡，并研究了涉及 miR-124-3p 和 PI3K/AKT 信号通路的调节机制。在 HBE 细胞中鹦鹉热衣原体感染后，我们观察到 HBE 细胞凋亡升高，伴随着 miR-124-3p 水平的上调。从机制上讲，我们将 EIF3B 鉴定为 miR-124-3p 的新型靶基因，其 mRNA 表达的负相关支持。miR-124-3p 抑制剂减少鹦鹉热衣原体诱导的细胞凋亡，增加鹦鹉热衣原体的复制并抑制 PI3K/AKT 激活，而 miR-124-3p 模拟物产生相反的作用，转染 EIF3B siRNA 逆转了 miR-124-3p 抑制剂的作用。我们的研究结果表明，靶向 EIF3B 的 miR-124-3p 通过激活 PI3K/AKT 信号通路促进鹦鹉热衣原体感染的 HBE 细胞凋亡。