Young V B, Knox K A, Schauer D B
Division of Bioengineering and Environmental Health, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Infect Immun. 2000 Jan;68(1):184-91. doi: 10.1128/IAI.68.1.184-191.2000.
Little is known about the molecular pathogenesis of hepatitis and enterocolitis caused by enterohepatic Helicobacter species. Sonicates of the murine pathogen Helicobacter hepaticus were found to cause progressive cell distension, accumulation of filamentous actin, and G(2)/M cell cycle arrest in HeLa cell monolayers. The genes encoding this cytotoxic activity were cloned from H. hepaticus. Three open reading frames with closest homology to cdtA, cdtB, and cdtC from Campylobacter jejuni were identified. Sonicates of a laboratory strain of Escherichia coli carrying the cloned cdtABC gene cluster from H. hepaticus reproduced the cytotoxic activities seen with sonicates of H. hepaticus. Cytolethal distending toxin activity is a potential virulence determinant of H. hepaticus that may play a role in the pathogenesis of Helicobacter-associated hepatitis and enterocolitis.
关于肝肠螺杆菌引起的肝炎和小肠结肠炎的分子发病机制,人们了解甚少。已发现鼠病原体肝螺杆菌的超声裂解物可导致HeLa细胞单层出现渐进性细胞膨胀、丝状肌动蛋白积累以及G(2)/M期细胞周期阻滞。编码这种细胞毒性活性的基因从肝螺杆菌中克隆出来。鉴定出了三个与空肠弯曲菌的cdtA、cdtB和cdtC具有最高同源性的开放阅读框。携带从肝螺杆菌克隆的cdtABC基因簇的实验室大肠杆菌菌株的超声裂解物重现了肝螺杆菌超声裂解物所具有的细胞毒性活性。细胞致死膨胀毒素活性是肝螺杆菌的一种潜在毒力决定因素,可能在螺杆菌相关肝炎和小肠结肠炎的发病机制中起作用。