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.
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