Takahashi S, Nakamura E, Okabe S
Department of Applied Pharmacology, Kyoto Pharmaceutical University, Yamashina, Japan.
Dig Dis Sci. 1998 Oct;43(10):2301-8. doi: 10.1023/a:1026635110099.
Cytokines are suspected to play a crucial role in the pathogenesis of Helicobacter pylori-associated gastric diseases. Hence, considerable attention has been paid to the actions of cytokines on gastric cells. We examined the effects of cytokines on mucus secretion by gastric epithelial cells, without or with H. pylori components. Mucus secretion by cultured gastric epithelial cells was assessed as secretion of [3H]glucosamine-prelabeled high-molecular-weight glycoproteins. Interleukin (IL)-1beta and IL-6 significantly stimulated mucus secretion, but other cytokines such as IL-7, IL-8, IL-10, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha had no effect. H. pylori lysate caused a decrease in both basal and stimulated secretion of mucus. In addition, IFN-gamma significantly potentiated the lysate-induced reduction of basal and stimulated secretion. Cell viability was not affected by any of treatments. These results indicate that IL-1beta and IL-6 stimulate mucus secretion, while IFN-gamma potentiates H. pylori-decreased secretion by gastric epithelial cells.
细胞因子被怀疑在幽门螺杆菌相关胃部疾病的发病机制中起关键作用。因此,细胞因子对胃细胞的作用已受到相当多的关注。我们研究了细胞因子对胃上皮细胞黏液分泌的影响,有无幽门螺杆菌成分的情况均进行了研究。培养的胃上皮细胞的黏液分泌通过[3H]葡萄糖胺预标记的高分子量糖蛋白的分泌来评估。白细胞介素(IL)-1β和IL-6显著刺激黏液分泌,但其他细胞因子如IL-7、IL-8、IL-10、干扰素(IFN)-γ和肿瘤坏死因子(TNF)-α则没有作用。幽门螺杆菌裂解物导致基础和刺激状态下的黏液分泌均减少。此外,IFN-γ显著增强了裂解物诱导基础和刺激状态下分泌减少的作用。细胞活力不受任何处理的影响。这些结果表明,IL-1β和IL-6刺激黏液分泌,而IFN-γ增强幽门螺杆菌导致的胃上皮细胞分泌减少。