Faculty of Biological Sciences, University of Leeds, Clarendon Road, Leeds LS2 9JT, United Kingdom.
Mol Immunol. 2011 Sep;48(15-16):2113-21. doi: 10.1016/j.molimm.2011.07.002. Epub 2011 Jul 30.
Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhoea in pigs and humans. The duration and severity of diarrhoea can be controlled using zinc supplementation, typically pharmacological levels of zinc oxide in pigs. In this study, IPEC J2 cells were used as an in vitro model of intestinal ETEC infection, with separate and simultaneous zinc treatment. Genomic analysis identified increased expression of a variety of innate immune response genes (NF-κB targets) in response to ETEC exposure, and several stress response genes in response to zinc exposure, provided as ZnO. Expression of genes involved in the innate immune response was reduced when cells were simultaneously exposed to ZnO, and it is suggested that ZnO treatment inhibits the induction of NF-κB in response to pathogens, possibly through up-regulated heat shock proteins. A similar response in vivo with consequent down-regulation in the inflammatory response would reduce further pathogen invasion, maintain normal gut function and maintain growth.
肠产毒性大肠杆菌（ETEC）是猪和人类腹泻的主要原因。通过补锌可以控制腹泻的持续时间和严重程度，通常在猪中使用氧化锌的药理水平。在这项研究中，IPEC J2 细胞被用作肠道 ETEC 感染的体外模型，进行单独和同时的锌处理。基因组分析确定，对 ETEC 暴露的反应中，多种先天免疫反应基因（NF-κB 靶标）的表达增加，对锌暴露的反应中，几种应激反应基因的表达增加，这些锌以氧化锌的形式提供。当细胞同时暴露于 ZnO 时，参与先天免疫反应的基因表达减少，并且据推测，ZnO 处理抑制了对病原体的 NF-κB 的诱导，可能是通过上调热休克蛋白。体内的类似反应会导致炎症反应的下调，从而减少进一步的病原体入侵，维持正常的肠道功能并保持生长。
