Effect of miR-155-5p/sirt1 signaling pathway on immune function of Candida albicans induced Kawasaki disease model mice

Acta Universitatis Medicinalis Anhui 2025 02 v.60 307-312+320     font:big middle small

Found programs: Basic Scientific Research Project of Liaoning Provincial Department of Education (No.LJKMZ20221229)

Authors:Wei Gang; Tian Jing; Liang Dongxue; Zhang Fengxiang; Chen Yue

Keywords:miR-155-5p;silent information regulator 1;Kawasaki disease;helper T cells 17;regulatory T cells;inflammation;immunity

DOI:10.19405/j.cnki.issn1000-1492.2025.02.017

〔Abstract〕 Objective To investigate the effect of the miR-155-5p/silent information regulator 1(sirt1) signaling pathway on the immune function ofCandida albicansinduced Kawasaki disease model mice. Methods C56BL/6 mice were separated into control group, Kawasaki disease group, antagonist control group, miR-155-5p antagonist group, miR-155-5p antagonist+si-NC group, and miR-155-5p antagonist+si-sirt1 group, with 12 mice in each group. Except for the control group, mice in all other groups were used to construct a Kawasaki disease model by intraperitoneal injection of water-solubleCandida albicans. After successful modeling, administration was performed once a day for 7 days. QRT-PCR was applied to detect the expression of miR-155-5p in coronary arteries. Western blot was applied to detect sirt1 protein in coronary arteries. HE staining was applied to detect pathological changes in coronary arteries. Mouse thymus index and spleen index were detected. Flow cytometry was applied to detect helper T cells 17(Th17)/regulatory T cells(Treg) in peripheral blood. ELISA was applied to detect the levels of interleukin(IL)-17 and IL-10 in mouse serum. The targeting relationship between sirt1 and miR-155-5p was validated. Results Compared with the control group, there was a large amount of inflammatory cell infiltration in the coronary arteries of mice in the Kawasaki disease group. The miR-155-5p expression, Th17 ratio, Th17/Treg ratio, and IL-17 level increased. The sirt1 protein expression, thymus index, spleen index, Treg ratio, and IL-10 level decreased(P<0.05). Compared with the Kawasaki disease group, the inflammatory cell infiltration in the coronary arteries of mice in the miR-155-5p antagonist group was alleviated. The miR-155-5p expression, Th17 ratio, Th17/Treg ratio, and IL-17 level decreased. The sirt1 protein expression, thymus index, spleen index, Treg ratio, and IL-10 level increased(P<0.05). Si-sirt1 weakened the promoting effect of miR-155-5p inhibition on Th17/Treg balance and the inhibitory effect on vascular inflammation in Kawasaki disease mice, miR-155-5p targeted and regulated sirt1. Conclusion The mechanism by which inhibiting miR-155-5p promotes Th17/Treg balance and inhibits vascular inflammation in Kawasaki disease mice may be related to the upregulation of sirt1 expression.