Fu Qiang, Zhu Xingyuan, Fang Qiongyan, Han Hui, Wang Zhiying, Xie Jinye, Qian Dong, Wu Xinger, Wu Yongjian, Chen Kang
Zhongshan Cancer Research Institute of Zhongshan City, Zhongshan City People's Hospital, Zhongshan, Guangdong, 528403, China.
Center for Infection and Immunity, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong Province, 519000, China.
Heliyon. 2024 Aug 20;10(17):e36585. doi: 10.1016/j.heliyon.2024.e36585. eCollection 2024 Sep 15.
Keratitis induced by (. ) is an acute and serious corneal inflammation. As a family of gene regulators, miRNAs play a crucial role in modulating host response after microbial invasion. However, their functions in . keratitis remain largely unclear. In the present study, we demonstrated that miR-155 expression was significantly increased in macrophages and corneal tissue after . infection. studies demonstrated that mice with miR-155 knockdown displayed more resistance to keratitis, with a lower bacterial burden. In addition, and studies indicated that miR-155 enhanced apoptosis of macrophages after infection, and resulted in a susceptible phenotype of keratitis. Moreover, miR-155 induced apoptosis through reducing activation of PI3K-Akt signaling pathway. Our data provided evidence of miR-155 mediated apoptosis of macrophage in keratitis, which may be an underlying target for the therapy of keratitis and other infectious diseases.
由（.）引起的角膜炎是一种急性严重的角膜炎症。作为基因调节因子家族，微小RNA（miRNAs）在微生物入侵后调节宿主反应中起关键作用。然而，它们在.角膜炎中的功能仍 largely不清楚。在本研究中，我们证明在.感染后巨噬细胞和角膜组织中miR-155表达显著增加。研究表明，miR-155敲低的小鼠对.角膜炎表现出更强的抵抗力，细菌载量更低。此外，.和.研究表明，miR-155在.感染后增强巨噬细胞凋亡，并导致.角膜炎的易感表型。此外，miR-155通过降低PI3K-Akt信号通路的激活诱导凋亡。我们的数据提供了miR-155介导.角膜炎中巨噬细胞凋亡的证据，这可能是.角膜炎和其他传染病治疗的潜在靶点。
