人类结肠共生产肠毒素脆弱拟杆菌 (ETBF) 与慢性结肠炎和结肠癌有关。 ETBF 定植通过脆弱拟杆菌毒素 (BFT) 诱发结肠炎。 ETBF 分泌的 BFT 通过 E-钙粘蛋白裂解/NF-κB 信号传导引起结肠炎症。 ETBF 通过白细胞介素 17A (IL-17A)/CXCL 依赖性炎症促进结肠肿瘤发生，但其在 ETBF 促进肿瘤发生中的生物活性疗法仍未被探索。在当前的研究中，我们研究了 ETBF 结肠炎和肿瘤发生小鼠模型中的咖啡酸苯乙酯 (CAPE)。在这项研究中，我们观察到 CAPE 治疗减轻了 ETBF 引起的小鼠炎症。此外，我们的研究结果表明，在由氧化偶氮甲烷 (AOM) 和葡聚糖硫酸钠诱导的结肠炎相关结肠癌小鼠模型中，CAPE 治疗对 ETBF 增强的结肠肿瘤发生具有保护作用。值得注意的是，CAPE 给药后结肠肿瘤发生的减少与胃肠道中 IL-17A 和 CXCL1 表达的减少相关。 CAPE 诱导的针对 ETBF 介导的肿瘤发生的保护作用的分子机制是由 IL-17A/CXCL1 以及肠上皮细胞中的 NF-κB 活性介导的。我们的研究结果表明，CAPE 可以作为预防剂，预防 ETBF 诱导的结肠炎和结直肠癌 (CRC) 的发展。

The human colonic commensal enterotoxigenic Bacteroides fragilis (ETBF) is associated with chronic colitis and colon cancer. ETBF colonization induces colitis via the Bacteroides fragilis toxin (BFT). BFT secreted by ETBF cause colon inflammation via E-cadherin cleavage/NF-κB signaling. ETBF promotes colon tumorigenesis via interleukin 17A (IL-17A)/CXCL-dependent inflammation, but its bioactive therapeutics in ETBF-promoted tumorigenesis remain unexplored. In the current study, we investigated the caffeic acid phenethyl ester (CAPE) in the murine model of ETBF colitis and tumorigenesis. In this study, we observed that CAPE treatment mitigated inflammation induced by ETBF in mice. Additionally, our findings indicate that CAPE treatment offers protective effects against ETBF-enhanced colon tumorigenesis in a mouse model of colitis-associated colon cancer induced by azoxymethane (AOM) and dextran sulfate sodium. Notably, the decrease in colon tumorigenesis following CAPE administration correlates with a reduction in the expression of IL-17A and CXCL1 in the gastrointestinal tract. The molecular mechanism for CAPE-induced protection against ETBF-mediated tumorigenesis is mediated by IL-17A/CXCL1, and by NF-κB activity in intestinal epithelial cells. Our findings indicate that CAPE may serve as a preventive agent against the development of ETBF-induced colitis and colorectal cancer (CRC).