Feng Na, Zhi Dejuan, Zhang Liyun, Tian Jing, Ren Hui, Li Chanhe, Zhu Hongmei, Li Hongyu
Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, MOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, PR China.
Institute of Microbiology and Biochemical Pharmacy, School of Pharmacy, Lanzhou University, Lanzhou 730000, PR China.
Biochem Biophys Res Commun. 2015 Apr 10;459(3):481-7. doi: 10.1016/j.bbrc.2015.02.132. Epub 2015 Mar 5.
Both mutation and knockdown in mev-1 gene render Caenorhabditis elegans susceptibility to Enterococcus faecalis infection. However, the mechanisms by which of MEV-1 defects pathogen resistance remain unclear. Here we show that mev-1RNAi causes a dramatic decrease in oxidative stress and antioxidant enzyme expressions, thereby leading to increased E. faecalis accumulation in nematode intestine. Mitochondrial superoxide change after infection induced these oxidative responses through DAF-16 activity. All together, this highlights MEV-1 as a key regulatory component for determining genetic responsiveness to oxidant/antioxidant imbalance that is associated with innate immunity.
mev-1基因的突变和敲低都会使秀丽隐杆线虫易受粪肠球菌感染。然而，MEV-1缺陷影响病原体抗性的机制仍不清楚。在此我们表明，mev-1RNA干扰导致氧化应激和抗氧化酶表达显著降低，从而导致粪肠球菌在线虫肠道中的积累增加。感染后线粒体超氧化物变化通过DAF-16活性诱导了这些氧化反应。总之，这突出了MEV-1作为决定与先天免疫相关的氧化/抗氧化失衡遗传反应性的关键调节成分。
