Sittipo Panida, Lobionda Stefani, Choi Kyungchul, Sari Ita Novita, Kwon Hyog Young, Lee Yun Kyung
Soonchunhyang Institute of Medi-Bio Science, Soonchunhyang University, Cheonan, South Korea.
Front Microbiol. 2018 Jul 17;9:1588. doi: 10.3389/fmicb.2018.01588. eCollection 2018.
The beneficial role of gut microbiota in intestinal diseases has been highlighted recently. found in the human gastrointestinal tract is a well-studied example of a beneficial bacterium that protects against intestinal inflammation. Polysaccharide A (PSA) from induces the production of interleukin (IL)-10 from immune cells via Toll-like receptor 2 (TLR2) signaling in animal colitis models. The direct effect of PSA on human colorectal cancer (CRC) cells has not been studied. Here, we report the effect of PSA from on CRC pathogenesis in SW620 and HT29 CRC cells and the molecular signaling underlying these effects. We demonstrated that PSA induced the production of the pro-inflammatory cytokine, IL-8, but not IL-10, in CRC cells. PSA inhibited CRC cell proliferation by controlling the cell cycle and impaired CRC cell migration and invasion by suppressing epithelial mesenchymal transition. Moreover, as in the case of other animal intestinal diseases, the protective role of PSA against CRC pathogenesis was also mediated by TLR2. Our results reveal that PSA from plays a protective role against CRC via TLR2 signaling.
肠道微生物群在肠道疾病中的有益作用最近得到了凸显。在人类胃肠道中发现的一种经过充分研究的有益细菌是预防肠道炎症的典型例子。在动物结肠炎模型中，来自该细菌的多糖A（PSA）通过Toll样受体2（TLR2）信号传导诱导免疫细胞产生白细胞介素（IL）-10。PSA对人结肠直肠癌（CRC）细胞的直接作用尚未得到研究。在此，我们报告了来自该细菌的PSA对SW620和HT29 CRC细胞中CRC发病机制的影响以及这些影响背后的分子信号传导。我们证明，PSA在CRC细胞中诱导促炎细胞因子IL-8的产生，但不诱导IL-10的产生。PSA通过控制细胞周期抑制CRC细胞增殖，并通过抑制上皮间质转化损害CRC细胞的迁移和侵袭。此外，与其他动物肠道疾病的情况一样，PSA对CRC发病机制的保护作用也由TLR2介导。我们的结果表明，来自该细菌的PSA通过TLR2信号传导对CRC发挥保护作用。
