Nakamura Yoshihiro, Sakagami Takashi, Yamamoto Noriyasu, Yokota Yoshiro, Koizuka Hiromasa, Hori Kazutoshi, Fukuda Yoshihiro, Tanida Noritoshi, Kobayashi Takehiko, Shimoyama Takashi
Department of Gastroenterology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
Jpn J Cancer Res. 2002 Feb;93(2):111-6. doi: 10.1111/j.1349-7006.2002.tb01248.x.
Helicobacter pylori (H. pylori) infection has been acknowledged as a promoter and an initiator for gastric carcinogenesis in experimental models using Mongolian gerbils with H. pylori strains TN2GF4 and ATCC 43504, which have + ve cagA and vacA phenotype s1 / m1. To get more insight into the role of H. pylori in gastric carcinogenesis, we studied the effect of H. pylori SS1, which has + ve cagA and vacA phenotype s2 / m2, on N-methyl-N-nitrosourea (MNU)-induced chemical gastric carcinogenesis using SPF C57BL / 6 mice. Thus, H. pylori SS1 was inoculated 1 week after the completion of MNU treatment to examine the promoting effect of this bacterium. The incidences of polypoid lesions, differentiated adenocarcinomas, and adenomatous hyperplasias were 67% (10 / 15), 47% (7 / 15) and 80% (12 / 15), respectively, in the MNU-alone group. The corresponding figures were 31% (8 / 26), 23% (6 / 26) and 35% (9 / 26) in the MNU + H. pylori group. The incidences of polypoid lesions and adenomatous hyperplasia were significantly different between the groups. Thus, the results indicate that H. pylori SS1 infection reduced susceptibility to chemical gastric carcinogenesis in this model. The discrepancy between the present result and previous results is likely to have been caused by differences in host factors and bacterial factors. Further study of the relationship between gastric carcinogenesis and H. pylori infection is needed.
在使用带有幽门螺杆菌菌株TN2GF4和ATCC 43504（具有cagA阳性和vacA表型s1/m1）的蒙古沙鼠的实验模型中，幽门螺杆菌（H. pylori）感染已被公认为是胃癌发生的促进因素和起始因素。为了更深入了解幽门螺杆菌在胃癌发生中的作用，我们使用无特定病原体的C57BL/6小鼠，研究了具有cagA阳性和vacA表型s2/m2的幽门螺杆菌SS1对N-甲基-N-亚硝基脲（MNU）诱导的化学性胃癌发生的影响。因此，在MNU治疗完成1周后接种幽门螺杆菌SS1，以检查该细菌的促进作用。仅接受MNU处理的组中，息肉样病变、分化型腺癌和腺瘤样增生的发生率分别为67%（10/15）、47%（7/15）和80%（12/15）。在MNU+幽门螺杆菌组中，相应的数据分别为31%（8/26）、23%（6/26）和35%（9/26）。两组之间息肉样病变和腺瘤样增生的发生率有显著差异。因此，结果表明在该模型中，幽门螺杆菌SS1感染降低了对化学性胃癌发生的易感性。目前的结果与先前结果之间的差异可能是由宿主因素和细菌因素的差异引起的。需要进一步研究胃癌发生与幽门螺杆菌感染之间的关系。
