| Literature DB >> 35157222 |
Xiaohua Li1,2, Yuanzhong Gong3, Xin Lin1, Qiong Lin1, Jianxiong Luo1, Tianxing Yu1, Junping Xu1, Lifang Chen1, Liyu Xu4, Ying Hu5.
Abstract
Acute lung injury caused by Candida albicans could result in high mortality and morbidity. MicroRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) have been believed to play a key in the regulation of inflammatory response. Whether miR-155/SOCS1 axis could regulate the acute lung injury caused by C. albicans has not been reported. The acute lung injury animal model was established with acute infection of C. albicans. miR-155 inhibitor, miR-155 mimic, and sh-SOCS1 were constructed. The binding site between miR-155 and SOCS1 was identified with dual luciferase reporter assay. Knockdown of miR-155 markedly inhibited the germ tube formation of C. albicans. Knockdown of miR-155 significantly up-regulated the expression of SOCS1, and the binding site between miR-155 and SOCS1 was identified. Knockdown of miR-155 improved the acute lung injury, suppressed inflammatory factors and fungus loading through SOCS1. Knockdown of SOCS1 greatly reversed the influence of miR-155 inhibitor on the cell apoptosis in vitro. The improvement of acute lung injury caused by C. albicans, suppression of inflammatory response and C. albicans infection, and inhibitor of cell apoptosis were achieved by knocking down miR-155 through SOCS1. This research might provide a new thought for the prevention and treatment of acute lung injury caused by C. albicans through targeting miR-155/SOCS1 axis.Entities:
Keywords: Candida albicans; SOCS1; acute lung injury; miR-155
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Year: 2022 PMID： 35157222 PMCID： PMC8853013 DOI： 10.1007/s12275-022-1663-5
Source DB: PubMed Journal: J Microbiol ISSN： 1225-8873 Impact factor: 2.902