Antibody and cytokine responses in Helicobacter pylori-infected various mouse strains.
Antibody and cytokine responses in Helicobacter pylori-infected various mouse strains.
复制标题
幽门螺杆菌感染的各种小鼠品系的抗体和细胞因子反应。
作者：
A. Dey;K. Yokota;K. Kobayashi;K. Oguma;Y. Hirai;T. Akagi
幽门螺杆菌(Hp)感染与慢性活动性胃炎、消化性溃疡、胃癌和胃粘膜相关淋巴组织淋巴瘤的病因学密切相关。在本研究中，我们检测了三个品系的小鼠(BALB/c、C3H/He和C57BL/6)感染幽门螺杆菌后的抗体反应和细胞因子谱。随后对宿主免疫反应与炎症强度的相关性进行了分析。幽门螺杆菌(ATCC43504)从4周龄开始每周灌胃给药1次，分别于4、7个月龄处死。在这些小鼠中，我们检查了胃的组织学、抗幽门螺杆菌的抗体效价和血清细胞因子(IL-4、IL-10、TNF-α、IL-2和干扰素-γ)的水平。在BALB/c小鼠中，胃部炎症轻微。63.6%的C57BL/6小鼠和33.3%的C3H/He小鼠出现炎症反应。在C57BL/6和C3H/He小鼠中，所有细胞因子均有升高的趋势。相比之下，BALB/c小鼠除了IL-2外，在细胞因子的产生方面不活跃。两只C3H/He小鼠出现了严重的淋巴滤泡炎症；一只表现出典型的Th-1反应，另一只表现出典型的Th-2反应。虽然用细胞因子的产生来评价Th-1/Th-2应答与炎症强度之间没有明确的相关性，但似乎在Hp诱导的炎症中，细胞免疫(Th-1)和体液免疫(Th-2)都在发病机制中发挥了作用。
Helicobacter pylori (H. pylori) infection in the stomach is etiologically closely associated with chronic active gastritis, peptic ulcer, gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma. In this study, we examined the antibody responses and cytokine profiles of three strains of mice (BALB/c, C3H/He, and C57BL/6) infected with H. pylori. Following this, correlations between host-immune reactions and intensity of inflammation were analyzed. H. pylori (ATCC43504) was intragastrically administered once a week to the mice from 4 weeks of age, and they were sacrificed at the ages of 4 and 7 months. In these mice, we examined the histology of the stomach, antibody titers against H. pylori, and serum levels of cytokines (IL-4, IL-10, TNF-alpha, IL-2 and Interferon-gamma). In BALB/c mice, inflammation of the stomach was minimal. Inflammation was observed in 63.6% of C57BL/6 mice and 33.3% of C3h/He mice. In C57BL/6 and C3H/He mice, all the cytokines tended to increase. In contrast, BALB/c mice were inactive in cytokine production except for IL-2. Two C3H/He mice developed severe inflammation with lymph follicles; one showed a response largely typical of Th-1, and the other showed a response largely typical of Th-2. Although a definite correlation was not shown between Th-1/Th-2 response evaluated by cytokine production and intensity of inflammation, it appears that in H. pylori-induced inflammation both cell-mediated (Th-1) and humoral (Th-2) immunity play a role in pathogenesis.