Byrd J C, Yunker C K, Xu Q S, Sternberg L R, Bresalier R S
Gastrointestinal Cancer Research Laboratory, Henry Ford Health Sciences Center, Detroit, Michigan, USA.
Gastroenterology. 2000 Jun;118(6):1072-9. doi: 10.1016/s0016-5085(00)70360-x.
BACKGROUND & AIMS: Mucins are high-molecular-weight glycoproteins that protect the gastric epithelium. Previous data suggested that gastric surface-type mucin is decreased in Helicobacter pylori-infected patients and restored after eradication of the infection. Our aim was to determine the effect of H. pylori on mucin synthesis in cultured gastric epithelial cells.
Mucin synthesis was measured by labeling with [(3)H]glucosamine and size-exclusion chromatography. Expression of MUC5AC and MUC1 mucin protein antigens was quantitated by Western blot analysis.
Mucin synthesis was inhibited more than 80% when KATO III cells were incubated with H. pylori, with no effect on mucin secretion or degradation. Inhibition was rapid (4 hours), partially reversible, dependent on concentration of bacteria, and associated with the insoluble membrane fraction. H. pylori decreased levels of MUC5AC and MUC1 mucins. MUC1 inhibition was half-maximal by 4 hours and partially reversed by 24 hours, but the decrease in MUC5AC was less rapid and not reversible within 24 hours.
H. pylori inhibits total mucin synthesis in vitro and decreases the expression of MUC5AC and MUC1. A decrease in gastric mucin synthesis in vivo may disrupt the protective surface mucin layer.
黏蛋白是保护胃上皮的高分子量糖蛋白。先前的数据表明,幽门螺杆菌感染患者的胃表面型黏蛋白减少,感染根除后恢复。我们的目的是确定幽门螺杆菌对培养的胃上皮细胞中黏蛋白合成的影响。
通过用[³H]葡糖胺标记和尺寸排阻色谱法测量黏蛋白合成。通过蛋白质印迹分析定量MUC5AC和MUC1黏蛋白蛋白抗原的表达。
当KATO III细胞与幽门螺杆菌一起孵育时,黏蛋白合成被抑制超过80%,对黏蛋白分泌或降解没有影响。抑制作用迅速(4小时),部分可逆,取决于细菌浓度,并与不溶性膜部分相关。幽门螺杆菌降低了MUC5AC和MUC1黏蛋白的水平。MUC1的抑制在4小时时达到半数最大效应,24小时时部分逆转,但MUC5AC的降低速度较慢,在24小时内不可逆。
幽门螺杆菌在体外抑制总黏蛋白合成,并降低MUC5AC和MUC1的表达。体内胃黏蛋白合成的减少可能会破坏保护性表面黏蛋白层。