【作者】 仵雁北； 王静； 何强； Liangli (Lucy) Yu； Quynhchi Pham； Lumei Cheung； Young S.Kim； Thomas T.Y.Wang； Allen D.Smith；

【Author】 Wu Yanbei;Wang Jing;He Qiang;Liangli Yu;Quynhchi Pham;Lumei Cheung;Young S.Kim;Thomas T.Y.Wang;Allen D.Smith;School of Food Science and Health,Beijing Technology & Business University;Beltsville Human Nutrition Research Center,United State Department of Agriculture;College of Biomass Science and Engineering,Sichuan University;Department of Nutrition and Food Science,University of Maryland;Division of Cancer Prevention,National Cancer Institute;

【机构】 北京工商大学食品与健康学院； 美国农业部贝兹维尔人类研究中心； 四川大学轻工科学与工程学院； 马里兰大学营养与食品科学学院； 美国国家癌症研究所癌症预防部门；

【摘要】 肠致病性和肠出血性大肠杆菌是导致人类出血性结肠炎甚至致命的溶血性尿毒症综合征的重要肠道病原体。有研究表明,十字花科蔬菜的重要衍生物吲哚-3-甲醇有望克服多重耐药性,成为对抗大肠杆菌感染的抗生素替代品,但其作用机制尚不清晰。因此,本文采用啮齿柠檬酸杆菌(Citrobbacter rodentium,Cr)感染模拟致病性大肠杆菌诱导的急性肠道炎症,研究食源性吲哚-3-甲醇(I3C)对Cr敏感的C3H/HeN小鼠免疫反应的影响。结果显示,食用1μmol I3C/g饮食可显著抑制Cr感染小鼠体重的减轻和脾脏重量的增加,但对小鼠粪便和结肠中的Cr定植量没有影响,表明I3C不能阻止Cr在易感型小鼠肠道中的入侵和定殖,但可减轻Cr感染引起的小鼠生理变化和组织损伤。我们还发现I3 C通过维持Cr感染小鼠结肠中的抗炎细胞因子IL-22 mRNA水平,同时减少其它促炎细胞因子(包括IL17A,IL6,IL1β,TNF-α,IFN-γ)的表达,以降低C3H/HeN小鼠对Cr感染的炎症反应。此外,饮食中的I3C还显著地降低了感染小鼠血清中IL17,TNF-α,IL12p70和G-CSF的细胞因子水平,并特异性地增强了其IgG反应,进一步的证实了食源性I3 C对细菌感染小鼠的免疫调节作用。更多还原

【Abstract】 Enteropathogenic and enterohemorrhagic Escherichia coli are important enteric pathogens that induce hemorrhagic colitis or even fatal hemolytic uremic syndrome.Emerging evidence shows that Indole-3-carbinal(I3 C),a bioactive compound bioactive compound derived from cruciferous vegetables,is expected to be an alternative of antibiotics against the E.coli infection for overcoming multidrug resistant.In this study,Citrobacter rodentium(Cr) infection model was utilized to mimic E.coli-induced acute intestinal inflammation,and the effects of a cruciferous vegetable-derived cancer protective compound,indole-3-carbinol(I3 C),on the immune responses of Cr-susceptible C3 H/HeN mice were investigated.The results showed that dietary I3 C significantly inhibited the loss of body weight and the increase of spleen weight in the mice infected with Cr,but has no effect on the amount of Cr in feces and colon in mice,indicating that I3 C could not prevent susceptible mice from Cr invasion and colonization but alleviated the physiological changes and tissue damage induced by Cr infection.In addition,13 C treatment reduced the inflammatory response to Cr infection by maintaining anti-inflammatory cytokine IL-22 mRNA levels while reducing expression of other pro-inflammatory cytokines including IL17 A,IL6,IL1β,TNF-α,IFN-γ.Moreover,the serum cytokine levels of IL17,TNF-α,IL12 p70 and G-CSF in serum also was down-regulated by I3 C in Cr-infected mice.Additionally,dietary I3 C specifically enhanced the Cr-specific IgG response to Cr infection,which further confirmed the immunoregulatory effects of I3 C on C3 H/HeN mice infected by Citrobacter rodentium.更多还原