Establishment of Helicobacter pylori infection models in rats and mice

本研究旨在建立大鼠和小鼠幽门螺杆菌感染模型。一次性口服接种vaca和caga阳性幽门螺杆菌菌株（ATCC43504）。正常Donryu、Sprague-Dawley和Wistar大鼠未见幽门螺杆菌感染。胃溃疡大鼠（Donryu品系）感染幽门螺杆菌。胃溃疡可自行愈合，但幽门螺杆菌感染往往会损害溃疡愈合。胃中幽门螺杆菌的数量随着溃疡的愈合而减少。同样，hcl诱导粘膜病变的大鼠（Sprague-Dawley菌株）感染幽门螺杆菌。幽门螺杆菌数量与病灶面积有关，随病灶愈合而减少。幽门螺杆菌感染不影响愈合。另一方面，在正常小鼠中，幽门螺杆菌持续在胃粘膜定植至少26周。阿莫西林、克拉霉素等抗生素可降低幽门螺杆菌数量，而联合质子泵抑制剂（奥美拉唑、兰索拉唑）的抗生素更能显著降低胃内幽门螺杆菌活力。幽门螺旋杆菌感染引起的胃炎伴炎性细胞浸润，但与幽门螺旋杆菌感染的人和蒙古沙鼠相比，胃病理较轻。即使在幽门螺杆菌感染的小鼠用阿司匹林治疗后，病理也没有得到很大的改善。幽门螺杆菌感染小鼠未发生胃溃疡。

This study was designed to establish Helicobacter pylori (H.pylori) infection models in rats and mice. H.pylori of VacA-and CagA-positive strain (ATCC43504) was once orally inoculated to the animals. H.pylori infection was not observed in normal Donryu, Sprague-Dawley or Wistar rats. In contrast, the rats (Donryu strain) with gastric ulcers were infected with H.pylori. Gastric ulcers spontaneously healed, but H.pylori infection tended to impaire ulcer healing. The number of H.pylori in the stomach decreased with ulcer healing. Similarly, the rats (Sprague-Dawley strain) with HCl-induced mucosal lesions were infected with H.pylori. The number of H.pylori was associated with lesion area and decreased with the healing of the lesions. H.pylori infection did not affect the healing. On the other hand, in normal ddY mice, H.pylori persistently colonized the gastric mucosa for at least 26 weeks. The number of H.pylori was decreased by antibiotics such as amoxicillin and clarithromycin, and the antibiotics with proton pump inhibitors (omeprazole and lansoprazole) more profoundly reduced H.pylori viability in the stomach. H.pylori infection caused gastritis with inflammatory cell infiltration, but gastric pathology was mild, compared with those in H.pylori-infected humans and Mongolian gerbils. Even after H.pylori-infected mice were treated with aspirin, the pathology was not largely promoted. Gastric ulcers did not occur in H.pylori-infected mice.