现代检验医学杂志2025，Vol.40Issue(6)：33-37,5.DOI:10.3969/j.issn.1671-7414.2025.06.007
TIM-3通过Galectin-3调控M2型巨噬细胞极化在小鼠肺炎链球菌肺炎肺损伤中作用机制研究
Mechanism of TIM-3 Regulating M2 Macrophage Polarization through Galectin-3 in Mice Streptococcals Pneumoniae Pneumonia
摘要
Abstract
Objective To explore the possible mechanism of T cell immunoglobulin and mucin domain-containing protein-3(TIM-3)regulating M2 macrophage polarization through Galectin-3 in lung injury induced by Streptococcals pneumoniae pneumonia(SPP)in mice.Methods Thirty mice were divided into control group,SPP group and SPP+TIM-3 inhibition group,with 10 mice in each group.The macrophage cell line RAW 264.7 was cultured and divided into a control group,with the SPP group versus the SPP+TIM-3 inhibition group.Lung histopathology was detected by hematoxylin-eosin(H&E)staining.Serum and cell supernatant tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and IL-6 content were measured by enzyme-linked immunosorbent assay(ELISA).Western blotting the protein levels of TIM-3 and Galectin-3 were determined in lung tissues and macrophages.Cluster of differentiation(CD)206,CD86 mRNA levels in lung tissue and macrophages were determined by real time quantitative PCR(RT-qPCR).Results Compared with the control group,the SPP group had significantly abnormal lung tissue pathological structure,thickened alveolar septum,a large number of inflammatory cells infiltration,a large amount of exudate in alveolar space,and increased serum inflammatory factors TNF-α,IL-6 and IL-1β,the protein and mRNA expressions of CD86,the marker protein of M1 macrophages,and the protein and mRNA expressions of CD206,the marker protein of M2 macrophages,and the protein expressions of TIM-3 and Galectin-3 in lung tissues were significantly increased in the model group,and the differences were statistically significally(t=8.36～76.30,all P<0.05).Compared with the SPP group,the SPP+TIM-3 inhibition group had improved lung tissue pathological damage,reduced alveolar septum thickness,inflammatory cell infiltration,reduced exudate in alveolar space,decreased serum inflammatory factors TNF-α,IL-6 and IL-1β content,and decreased expression of CD86 protein and mRNA in lung tissue.The expression of CD206 protein and mRNA was increased,the expression of TIM-3 protein was decreased,and the expression of Galectin-3 protein was increased,and the differences were statistically significant(t=10.67～63.32,all P<0.05).Cell experiments were consistent with this result.Conclusion Inhibition of TIM-3 can improve lung injury in SPP mice by down-regulating the expression of Galectin-3 and promoting M2 macrophage polarization.关键词
肺炎/肺炎链球菌/T细胞免疫球蛋白黏蛋白分子3/半乳糖凝集素-3/M2型巨噬细胞/极化Key words
pneumonia/Streptococcus pneumoniae/T cell immunoglobulin and mucin domain-containing protein 3/Galectin-3/M2 macrophages/polarization引用本文复制引用
余帮,张万巧,章晟,张悦..TIM-3通过Galectin-3调控M2型巨噬细胞极化在小鼠肺炎链球菌肺炎肺损伤中作用机制研究[J].现代检验医学杂志,2025,40(6):33-37,5.基金项目
北京市卫生健康委课题(2024-4-1111). （2024-4-1111）
