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

Acta Universitatis Medicinalis Anhui     font:big middle small

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

Authors:Wei Gang1 , 2 , 3 , Tian Jing4 , Liang Dongxue3 , 5 , Zhang Fengxiang1 , 2 , 3 , Chen Yue3 , 5

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〕 Abstract Objective To investigate the effect of the miR-155-5p/silent information regulator 1 (sirt1) signaling pathway on the immune function of Candida albicans induced 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-soluble Candida 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 vali- dated . 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 coro- nary 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 in- hibits vascular inflammation in Kawasaki disease mice may be related to the upregulation of sirt1 expression .