Laboratory of Systems Mucosal Biomodulation, Department of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea.
Toxicol Lett. 2012 Jun 20;211(3):289-95. doi: 10.1016/j.toxlet.2012.04.012. Epub 2012 Apr 26.
The widely used food additive carrageenan (CGN) has been shown to induce intestinal inflammation, ulcerative colitis-like symptoms, or neoplasm in the gut epithelia in animal models, which are also clinical features of human inflammatory bowel disease. In this study, the effects of CGN on pro-inflammatory transcription factors NF-κB and early growth response gene 1 product (EGR-1) were evaluated in terms of human intestinal epithelial barrier integrity. Both pro-inflammatory transcription factors were elevated by CGN and only NF-κB activation was shown to be involved in the induction of pro-inflammatory cytokine interleukin-8. Moreover, the integrity of the in vitro epithelial monolayer under the CGN insult was maintained by both activated pro-inflammatory transcription factors NF-κB and EGR-1. Suppression of NF-κB or EGR-1 aggravated barrier disruption by CGN, which was associated with the reduced gene expression of tight junction component zonula occludens 1 and its irregular localization in the epithelial monolayer.
食品添加剂卡拉胶（CGN）在动物模型中已被证实可诱导肠道炎症、溃疡性结肠炎样症状或肿瘤，这些也是人类炎症性肠病的临床特征。在这项研究中，评估了 CGN 对人肠道上皮屏障完整性的促炎转录因子 NF-κB 和早期生长反应基因 1 产物（EGR-1）的影响。促炎转录因子均被 CGN 上调，且仅 NF-κB 激活被证明参与诱导促炎细胞因子白细胞介素-8 的产生。此外，CGN 刺激下体外上皮单层的完整性可通过激活的促炎转录因子 NF-κB 和 EGR-1 来维持。NF-κB 或 EGR-1 的抑制加重了 CGN 引起的屏障破坏，这与紧密连接成分闭合蛋白 1 的基因表达减少及其在上皮单层中的不规则定位有关。
