Snelling William J, Moran Anthony P, Ryan Kieran A, Scully Paul, McGourty Kieran, Cooney Jakki C, Annuk Heidi, O'Toole Paul W
Department of Microbiology and Alimentary Pharmabiotic Centre, University College Cork, Ireland.
Helicobacter. 2007 Jun;12(3):200-9. doi: 10.1111/j.1523-5378.2007.00499.x.
The Helicobacter pylori protein HorB (encoded by HP0127) is a member of a paralogous family that includes the adhesins BabA, AlpA, AlpB, and HopZ, which contribute to adhesion to gastric epithelial cells. Of the verified H. pylori porins, the HorB sequence is most similar to that of HopE, but the function of HorB is unknown. The aim of our study was to investigate the role of HorB in H. pylori gastric epithelial cell adhesion.
We disrupted the horB gene in H. pylori and measured the adhesion to gastric epithelial cells (AGS cells). We then assessed the effect that HorB disruption had on lipopolysaccharide (LPS) O-chain production and Lewis x and Lewis y antigen expression. A HorB mutant in the mouse-adapted strain H. pylori SS1 was created by marker exchange and mouse stomach colonization was quantified. Using reverse transcription polymerase chain reaction, human gastric biopsy material from H. pylori-infected patients was then examined for expression of the horB gene.
Disruption of the horB gene reduced H. pylori adhesion by more than twofold. Adhesion in the horB knockout strain was restored to wild-type levels by re-introduction of HorB into the chromosome. Disruption of HorB reduced production of LPS O-chains and lowered the level of expression of Lewis x and Lewis y antigens. Insertional mutagenesis of the horB gene in H. pylori SS1 reduced mouse stomach colonization threefold. Finally, expression of the horB gene was detected in human gastric biopsy material from H. pylori-infected patients.
From these data we conclude that HorB has a role in H. pylori adhesion during infection.
幽门螺杆菌蛋白HorB(由HP0127编码)是一个旁系同源家族的成员,该家族包括黏附素BabA、AlpA、AlpB和HopZ,它们有助于幽门螺杆菌黏附于胃上皮细胞。在已证实的幽门螺杆菌孔蛋白中,HorB序列与HopE的序列最为相似,但HorB的功能尚不清楚。我们研究的目的是调查HorB在幽门螺杆菌黏附胃上皮细胞中的作用。
我们破坏了幽门螺杆菌中的horB基因,并检测其对胃上皮细胞(AGS细胞)的黏附情况。然后,我们评估了破坏HorB对脂多糖(LPS)O链产生以及Lewis x和Lewis y抗原表达的影响。通过标记交换在适应小鼠的幽门螺杆菌菌株SS1中创建了一个HorB突变体,并对小鼠胃定植情况进行了定量分析。然后,使用逆转录聚合酶链反应检测幽门螺杆菌感染患者的人胃活检材料中horB基因的表达情况。
horB基因的破坏使幽门螺杆菌的黏附能力降低了两倍多。通过将HorB重新导入染色体,horB基因敲除菌株的黏附能力恢复到了野生型水平。HorB的破坏减少了LPS O链的产生,并降低了Lewis x和Lewis y抗原的表达水平。在幽门螺杆菌SS1中对horB基因进行插入诱变使小鼠胃定植减少了三倍。最后,在幽门螺杆菌感染患者的人胃活检材料中检测到了horB基因的表达。
根据这些数据,我们得出结论,HorB在幽门螺杆菌感染过程中的黏附中发挥作用。