Dietary Salt Administration Decreases Enterotoxigenic Bacteroides fragilis (ETBF)-Promoted Tumorigenesis via Inhibition of Colonic Inflammation.
Dietary Salt Administration Decreases Enterotoxigenic Bacteroides fragilis (ETBF)-Promoted Tumorigenesis via Inhibition of Colonic Inflammation.
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DOI：
10.3390/ijms21218034
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发表时间：
2020-10-28
影响因子：
5.6
通讯作者：
Rhee KJ
中科院分区：
文献类型：
--
作者：
Hwang S;Yi HC;Hwang S;Jo M;Rhee KJ
西式饮食的消费与肠道微生物群介导的结肠炎症有关，这是结直肠癌的危险因素。高盐饮食（HSD）加剧炎症性肠病和其他自身免疫性疾病中IL-17 A诱导的炎症。产肠球菌性脆弱拟杆菌（ETBF）是一种肠道寄生菌，据报道其通过分泌脆弱拟杆菌毒素（BFT）而成为结肠炎的有效引发剂。BFT诱导结肠上皮细胞中E-钙粘蛋白的胞外域切割，从而导致细胞变圆、上皮屏障破坏和IL-8的分泌，其通过IL-17 A介导的炎症促进小鼠中的肿瘤发生。HSD是西式饮食的特征，可以表现出炎症作用。然而，HSD在ETBF诱导的结肠炎和肿瘤发生中诱导作用仍然未知。在这项研究中，我们研究了HSD对氧化偶氮甲烷（AOM）/葡聚糖硫酸钠（DSS）诱导肿瘤发生的ETBF定植小鼠以及ETBF结肠炎小鼠的影响。出乎意料的是，喂食HSD的ETBF感染的小鼠表现出减轻的体重减轻和脾肿大以及结肠炎症的减轻。HSD能显著降低ETBF感染小鼠结肠组织中IL-17 A和诱导型一氧化氮合酶（iNOS）的表达。此外，血清IL-17 A和一氧化氮（NO）水平也降低。然而，用氯化钠处理的HT 29/C1结肠上皮细胞显示BFT诱导的细胞变圆和IL-8表达没有变化。此外，HSD不影响ETBF在小鼠中的定殖。总之，HSD通过抑制IL-17 A和iNOS在结肠中的表达来减少ETBF诱导的肿瘤发生。HSD还抑制ETBF感染的AOM/DSS小鼠的结肠息肉数量。总之，这些发现表明，HSD消耗抑制ETBF促进的小鼠结肠癌发生，表明HSD在某些条件下可能具有有益作用。
Consumption of a Western-type diet has been linked to gut-microbiota-mediated colon inflammation that constitutes a risk factor for colorectal cancer. A high salt diet (HSD) exacerbates IL-17A-induced inflammation in inflammatory bowel disease and other autoimmune diseases. Enterotoxigenic Bacteroides fragilis (ETBF) is a gut commensal bacterium and reported to be a potent initiator of colitis via secretion of the Bacteroides fragilis toxin (BFT). BFT induces ectodomain cleavage of E-cadherin in colonic epithelial cells, consequently leading to cell rounding, epithelial barrier disruption, and the secretion of IL-8, which promotes tumorigenesis in mice via IL-17A-mediated inflammation. A HSD is characteristic of the Western-type diet and can exhibit inflammatory effects. However, a HSD induces effects in ETBF-induced colitis and tumorigenesis remain unknown. In this study, we investigated HSD effects in ETBF-colonized mice with azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced tumorigenesis as well as ETBF colitis mice. Unexpectedly, ETBF-infected mice fed a HSD exhibited decreased weight loss and splenomegaly and reduction of colon inflammation. The HSD significantly decreased the expression of IL-17A and inducible nitric oxide synthase (iNOS) in the colonic tissues of ETBF-infected mice. In addition, serum levels of IL-17A and nitric oxide (NO) were also diminished. However, HT29/C1 colonic epithelial cells treated with sodium chloride showed no changes in BFT-induced cellular rounding and IL-8 expression. Furthermore, HSD did not affect ETBF colonization in mice. In conclusion, HSD decreased ETBF-induced tumorigenesis through suppression of IL-17A and iNOS expression in the colon. HSD also inhibited colonic polyp numbers in the ETBF-infected AOM/DSS mice. Taken together, these findings suggest that a HSD consumption inhibited ETBF-promoted colon carcinogenesis in mice, indicating that a HSD could have beneficial effects under certain conditions.
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非毒性细菌片（NTBF）给药可降低细菌驱动的慢性结肠炎和肿瘤发育独立于多糖A。
影响因子：
8
作者：
Chan JL;Wu S;Geis AL;Chan GV;Gomes TAM;Beck SE;Wu X;Fan H;Tam AJ;Chung L;Ding H;Wang H;Pardoll DM;Housseau F;Sears CL
通讯作者：
Sears CL
影响因子：
30.3
作者：
Chung L;Thiele Orberg E;Geis AL;Chan JL;Fu K;DeStefano Shields CE;Dejea CM;Fathi P;Chen J;Finard BB;Tam AJ;McAllister F;Fan H;Wu X;Ganguly S;Lebid A;Metz P;Van Meerbeke SW;Huso DL;Wick EC;Pardoll DM;Wan F;Wu S;Sears CL;Housseau F
通讯作者：
Housseau F
影响因子：
8
作者：
通讯作者：
--
影响因子：
15.5
作者：
Miranda PM;De Palma G;Serkis V;Lu J;Louis-Auguste MP;McCarville JL;Verdu EF;Collins SM;Bercik P
通讯作者：
Bercik P
影响因子：
11.2
作者：
Housseau F;Wu S;Wick EC;Fan H;Wu X;Llosa NJ;Smith KN;Tam A;Ganguly S;Wanyiri JW;Iyadorai T;Malik AA;Roslani AC;Vadivelu JS;Van Meerbeke S;Huso DL;Pardoll DM;Sears CL
通讯作者：
Sears CL