D-Psicose intake exacerbates dextran sulfate sodium-induced colitis in mice through alteration in the gut microbiota and dysfunction of mucosal barrier

阿克曼西亚 结肠炎 肠道菌群 毛螺菌科 粘蛋白 促炎细胞因子 乳酸菌 炎症性肠病 内科学 免疫学 微生物学 化学 炎症 医学 生物 细菌 生物化学 疾病 厚壁菌 遗传学 16S核糖体RNA
作者
Xuejiao Zhang,Ang Li,Yuanyifei Wang,Jin Wang,Bowei Zhang,Yan Zhang,Jingmin Liu,Shuo Wang
标识
DOI:10.26599/fshw.2022.9250046
摘要

D-Psicose, as a low-calorie rare sugar, has attracted a lot of attention in recent years for alternating to sucrose. The anti-obesity effect of D-psicose has been extensively confirmed in previous studies, however, the impact of D-psicose on colitis remains vague. Here, we firstly evaluated the effect of the D-psicose prophylactic intervention on dextran sulfate sodium-induced colitis in C57BL/6 mice. The pathological symptoms, inflammatory cytokines levels, gut microbiota composition, short chain fatty acids (SCFAs) production and colonic barrier integrity were comprehensively evaluated. The results confirmed that D-psicose intervention aggravated colitis, characterized by the exacerbation of colon shortening, increase of colonic inflammatory infiltration, and marked exaltation of disease activity indices and IL-6, IL-1β and TNF-α levels. Further, the dysfunction of gut microbiota was identified in the psicose group. The abundance of pro-inflammatory bacteria Lachnospiraceae_NK4A136_group was significantly up-regulated while the abundance of probiotics Akkermansia and Lactobacillus were significantly down-regulated in the psicose group compared to the model group. Moreover, the production of SCFAs was suppressed in the psicose group, accompanied by a decrease in the level of mucin 2 (Muc-2). Collectively, the underlying mechanism of the exacerbation of colitis by D-psicose intervention might be attributed to microbiota dysfunction accompanied by the reduction of SCFAs, which leads to the damage of the mucosal barrier and the intensification of inflammatory invasion.
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