Belzer Clara, Stoof Jeroen, Beckwith Catherine S, Kuipers Ernst J, Kusters Johannes G, van Vliet Arnoud H M
Department of Gastroenterology and Hepatology, Erasmus MC - University Medical Center, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Department of Comparative Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Microbiology (Reading). 2005 Dec;151(Pt 12):3989-3995. doi: 10.1099/mic.0.28188-0.
Helicobacter hepaticus is a pathogen of rodents, which causes diverse enteric and hepatic inflammatory diseases and malignancies. The urease enzyme is an important colonization factor of gastric Helicobacter species like Helicobacter pylori, but little is known about the role and regulation of urease in enterohepatic Helicobacter species. Here it is reported that urease activity of H. hepaticus does not contribute to acid resistance, and that it is nickel-responsive at the post-translational level. H. hepaticus strain ATCC 51449 did not grow or survive at pH 3.0, and supplementation with urea or NiCl2 did not abrogate this acid sensitivity. Furthermore, urease enzyme activity of H. hepaticus was acid-independent, which contrasts with the acid-induced urease system of H. pylori. Nickel supplementation of Brucella medium resulted in a tenfold increase in urease activity in both H. hepaticus and H. pylori, but the maximum level of urease activity in H. hepaticus was still three- to fivefold lower when compared to H. pylori in the same conditions. The increase in urease activity of H. hepaticus was not associated with elevation of urease mRNA or protein levels. Inhibition of protein synthesis by chloramphenicol did not affect nickel-responsive induction of urease activity in H. hepaticus, and confirmed that nickel induction occurs at the post-translational level, probably by activation of preformed apo-enzyme. In conclusion, both the role of the urease enzyme and the regulation of urease activity differ between the enterohepatic pathogen H. hepaticus and the gastric pathogen H. pylori.
肝螺杆菌是啮齿动物的一种病原体，可引发多种肠道和肝脏炎症性疾病及恶性肿瘤。脲酶是幽门螺杆菌等胃螺杆菌的重要定植因子，但关于脲酶在肝肠螺杆菌属中的作用和调控知之甚少。本文报道，肝螺杆菌的脲酶活性对耐酸性无贡献，且在翻译后水平对镍有反应。肝螺杆菌菌株ATCC 51449在pH 3.0时无法生长或存活，添加尿素或氯化镍并不能消除这种酸敏感性。此外，肝螺杆菌的脲酶活性不依赖于酸，这与幽门螺杆菌的酸诱导脲酶系统形成对比。在布鲁氏培养基中添加镍可使肝螺杆菌和幽门螺杆菌的脲酶活性提高10倍，但在相同条件下，肝螺杆菌的脲酶活性最高水平仍比幽门螺杆菌低三至五倍。肝螺杆菌脲酶活性的增加与脲酶mRNA或蛋白质水平的升高无关。氯霉素抑制蛋白质合成并不影响镍对肝螺杆菌脲酶活性的诱导作用，并证实镍诱导发生在翻译后水平，可能是通过激活预先形成的脱辅基酶。总之，肝肠病原体肝螺杆菌和胃病原体幽门螺杆菌在脲酶的作用和脲酶活性的调控方面均存在差异。
