Cooksley Clare, Jenks Peter J, Green Andrew, Cockayne Alan, Logan Robert P H, Hardie Kim R
Institute of Infections and Immunity, Queen's Medical Centre, C-floor West Block, Nottingham NG7 2UH, UK 2Division of Gastroenterology, University Hospital, Nottingham NG7 2UH, UK 3School of Pharmaceutical Sciences, Nottingham University, Nottingham NG7 2RD, UK#dReceived 10 September 2002 Accepted 21 January 2003.
J Med Microbiol. 2003 Jun;52(Pt 6):461-469. doi: 10.1099/jmm.0.05070-0.
The Helicobacter pylori protein NapA has been identified as a homologue of the Escherichia coli protein Dps. It is shown in this study that, like Dps, NapA is produced maximally in stationary phase cells and contributes to the ability of H. pylori to survive under oxidative stress conditions. Moreover, NapA co-localizes with the nuclear material, suggesting that it can interact with DNA in vivo. Furthermore, it is demonstrated that repression of NapA production by iron starvation was not so pronounced in a H. pylori fur mutant, suggesting that the ferric uptake regulator (Fur) is involved in napA regulation, and a potential fur box by which this control could be mediated is identified. This finding is consistent with the regulation of iron-binding proteins by Fur and also the modulation of Fur during oxidative stress, thus allowing NapA levels to be increased in the environmental conditions under which its ability to protect DNA from attack by toxic free radicals is most beneficial to the cell.
幽门螺杆菌蛋白NapA已被鉴定为大肠杆菌蛋白Dps的同源物。本研究表明，与Dps一样，NapA在稳定期细胞中产量最高，并有助于幽门螺杆菌在氧化应激条件下存活的能力。此外，NapA与核物质共定位，表明它可以在体内与DNA相互作用。此外，还证明在幽门螺杆菌fur突变体中，铁饥饿对NapA产生的抑制作用不那么明显，这表明铁摄取调节因子（Fur）参与了napA的调节，并鉴定出了一个可能介导这种调控的潜在fur框。这一发现与Fur对铁结合蛋白的调节以及氧化应激期间Fur的调节相一致，从而使NapA水平在其保护DNA免受有毒自由基攻击的能力对细胞最有益的环境条件下得以增加。
