Zavros Y, Rieder G, Ferguson Amy, Merchant J L
Howard Hughes Medical Institute, University of Michigan, Ann Arbor, Michigan, USA.
Infect Immun. 2002 May;70(5):2630-9. doi: 10.1128/IAI.70.5.2630-2639.2002.
In mouse models and humans, Helicobacter pylori is associated with an increase in serum gastrin and gastrin-expressing (G) cells with a concomitant decrease in somatostatin-expressing D cells. Inflammation of the gastric mucosa can progress to metaplastic changes in the stomach and to decreased colonization by H. pylori and increased colonization by non-H. pylori organisms. In addition, about 20% of individuals with chronic gastritis are H. pylori negative, suggesting that other organisms may induce gastritis. Consistent with this hypothesis, we report here that Acinetobacter lwoffii causes the same histologic changes as does H. pylori. Gastric epithelial cells were isolated from the entire stomach by an enzymatic method for quantitation by both flow cytometry and morphometric analysis. Two months after mice were inoculated with H. pylori or A. lwoffii, the mucosal T- and B-cell numbers significantly increased. After 4 months of infection, there was a threefold increase in the number of G cells and a doubling in the number of parietal cells. A threefold decrease in the number of D cells occurred in H. pylori- and A. lwoffii-infected mice. Plasma gastrin levels increased after both H. pylori and A. lwoffii infection. Histology revealed the presence of inflammation in the gastric mucosa with both A. lwoffii and H. pylori infection. A periodic acid-Schiff stain-alcian blue stain revealed mucous gland metaplasia of the corpus. Collectively, the results demonstrate that gastritis and hypergastrinemia are not specific for H. pylori but can be induced by other gram-negative bacteria capable of infecting the mouse stomach.
在小鼠模型和人类中，幽门螺杆菌与血清胃泌素增加以及表达胃泌素的（G）细胞增多相关，同时表达生长抑素的D细胞减少。胃黏膜炎症可进展为胃化生改变，幽门螺杆菌定植减少，非幽门螺杆菌微生物定植增加。此外，约20%的慢性胃炎患者幽门螺杆菌检测呈阴性，提示其他微生物可能诱发胃炎。与此假设一致，我们在此报告，鲁氏不动杆菌引起的组织学变化与幽门螺杆菌相同。通过酶法从整个胃中分离胃上皮细胞，用于流式细胞术和形态计量分析定量。小鼠接种幽门螺杆菌或鲁氏不动杆菌两个月后，黏膜T细胞和B细胞数量显著增加。感染4个月后，G细胞数量增加了三倍，壁细胞数量增加了一倍。感染幽门螺杆菌和鲁氏不动杆菌的小鼠D细胞数量减少了三倍。幽门螺杆菌和鲁氏不动杆菌感染后血浆胃泌素水平均升高。组织学检查显示，鲁氏不动杆菌和幽门螺杆菌感染均导致胃黏膜出现炎症。过碘酸-希夫染色-阿尔辛蓝染色显示胃体部黏液腺化生。总体而言，结果表明胃炎和高胃泌素血症并非幽门螺杆菌所特有，其他能够感染小鼠胃部的革兰氏阴性菌也可诱发。
