Ohana M, Okazaki K, Oshima C, Kawasaki K, Fukui T, Tamaki H, Matsuura M, Asada M, Nishi T, Uchida K, Uose S, Nakase H, Iwano M, Matsushima Y, Hiai H, Chiba T
Department of Gastroenterology and Endoscopic Medicine, Kyoto University, Sakyo, Kyoto, 606-8507 Japan.
Gut. 2003 Aug;52(8):1102-10. doi: 10.1136/gut.52.8.1102.
Long term Helicobacter pylori infection leads to atrophic gastritis but the relation between H pylori infection and autoimmune related atrophic gastritis (AIG) remains unclear. We studied the effects of H pylori infection on the pathophysiology of AIG in mice.
BALB/c nu/nu mice (n=40) with or without H pylori infection received splenocytes from neonatally thymectomised mice to induce AIG. Half of the mice were orally infected with H pylori prior to AIG induction. Histological findings, and local and systemic immune responses were serially evaluated.
Two and six months after transfer, parietal cells in uninfected mice were depleted while those in infected mice were well preserved. The degree of gland atrophy (p<0.01), hyperplasia (p<0.01), gastric pH (p<0.05), and serum gastrin levels of infected mice were significantly lower than those of uninfected mice. Serum antiparietal cell antibody levels gradually decreased in infected mice, and were significantly lower than those of uninfected mice at six months (p<0.05). Real time polymerase chain reaction studies revealed significantly higher interleukin 4 (p<0.05) and transforming growth factor beta (p<0.05) gene expression in the gastric mucosa in infected mice than in uninfected mice at both two and six months after AIG induction.
H pylori infection inhibited the development of AIG in mice. Th2-type immune responses and transforming growth factor beta in the gastric microenvironment might be involved in the inhibitory effects of H pylori infection on the development of AIG, in which Th1-type responses have an important role.
长期幽门螺杆菌感染会导致萎缩性胃炎，但幽门螺杆菌感染与自身免疫性萎缩性胃炎（AIG）之间的关系仍不清楚。我们研究了幽门螺杆菌感染对小鼠AIG病理生理学的影响。
将有或无幽门螺杆菌感染的BALB/c裸鼠（n = 40）接受来自新生期胸腺切除小鼠的脾细胞以诱导AIG。一半小鼠在诱导AIG之前经口感染幽门螺杆菌。对组织学结果以及局部和全身免疫反应进行连续评估。
移植后2个月和6个月，未感染小鼠的壁细胞减少，而感染小鼠的壁细胞保存良好。感染小鼠的腺体萎缩程度（p<0.01）、增生程度（p<0.01）、胃pH值（p<0.05）和血清胃泌素水平均显著低于未感染小鼠。感染小鼠的血清抗壁细胞抗体水平逐渐降低，在6个月时显著低于未感染小鼠（p<0.05）。实时聚合酶链反应研究显示，在AIG诱导后2个月和6个月，感染小鼠胃黏膜中的白细胞介素4（p<0.05）和转化生长因子β（p<0.05）基因表达均显著高于未感染小鼠。
幽门螺杆菌感染抑制了小鼠AIG的发展。胃微环境中的Th2型免疫反应和转化生长因子β可能参与了幽门螺杆菌感染对AIG发展的抑制作用，其中Th1型反应起重要作用。
