同济大学学报（医学版）2025，Vol.46Issue(6)：804-810,7.DOI:10.12289/j.issn.2097-4345.25088
Flo8基因缺失白念珠菌甘露聚糖通过IL-10调控溃疡性结肠炎的机制研究
Mechanism of mannan from flo8-deficient Candida albicans in regulating ulcerative colitis via interleukin-10
摘要
Abstract
Objective To investigate the role and mechanism of mannan derived from flo8-deficient Candida albicans(flo8Δ-M)in regulating ulcerative colitis(UC)in a mouse model.Methods Mannan from C.albicans was extracted using a hot alkali method.The UC models were established in both wild-type(WT)and Clec4n knockout mice(Clec4n-/-).The mice were administered mannan via gavage at specified time points,and the weight changes,colon length and disease activity index(DAI)were monitored.The colonic levels of interleukin(IL)-6 and IL-10 were measured by enzyme-linked immunosorbent assay(ELISA).The bone marrow-derived dendritic cells(BMDCs)in the mice were stimulated with flo8Δ-M,and the IL-10 levels in the supernatant were quantified by ELISA.The phosphorylation of spleen tyrosine kinase(Syk)in BMDCs was assessed by Western blotting,and the IL-10 mRNA expression was determined by quantitative real-time polymerase chain reaction(qPCR).Results In vivo experiments demonstrated that flo8Δ-M gavage significantly increased the body weight,colon length,and IL-10 levels,while reduced the DAI and IL-6 levels in UC mice(all P＜0.05).In vitro experiments indicated that the flo8SΔ-M significantly induced IL-10 secretion in BMDCs via the Dectin-2-Syk signaling pathway(P＜0.05).The critical regulatory role of Dectin-2 was further validated in Clec4n knockout UC mice.Conclusion Mannan derived from flo8-deficient C.albicans exerts protective effects in UC mouse model by promoting anti-inflammatory cytokine IL-10 production through the Dectin-2-Syk signaling pathway.关键词
白念珠菌/flo8/甘露聚糖/溃疡性结肠炎/Dectin-2/小鼠Key words
Candida albicans/flo8/mannan/ulcerative colitis/Dectin-2/mice分类
医药卫生引用本文复制引用
朱方舟,杨宜衡,张思雨,贾鑫明..Flo8基因缺失白念珠菌甘露聚糖通过IL-10调控溃疡性结肠炎的机制研究[J].同济大学学报（医学版）,2025,46(6):804-810,7.基金项目
国家自然科学基金(82371777) （82371777）
