Salmonella enterica serovar Typhi modulates cell surface expression of its receptor, the cystic fibrosis transmembrane conductance regulator, on the intestinal epithelium
Salmonella enterica serovar Typhi modulates cell surface expression of its receptor, the cystic fibrosis transmembrane conductance regulator, on the intestinal epithelium
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DOI：
10.1128/iai.70.11.6416-6423.2002
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发表时间：
2002-11-01
影响因子：
3.1
通讯作者：
Pier, GB
中科院分区：
文献类型：
--
作者：
Lyczak, JB;Pier, GB
囊性纤维化跨膜传导调节因子（CFTR）蛋白是一种上皮受体，介导伤寒沙门氏菌向胃黏膜下层的移位。由于细胞表面CFTR的水平与伤寒沙门氏菌移位的效率直接相关，本研究的目的是测量感染期间肠道上皮细胞中CFTR的表达。上皮细胞胞质中原本存在的CFTR蛋白在接触活的伤寒沙门氏菌或细菌提取物后迅速转运至细胞膜。CFTR重新分布后，上皮细胞对细菌的摄取（依赖于CFTR）增加（>100倍）。触发CFTR重新分布的细菌因子对热和蛋白酶敏感。这些数据表明，伤寒沙门氏菌诱导肠道上皮细胞增加细胞膜上CFTR的水平，从而导致细菌摄入和黏膜下移位增强。这可能是导致伤寒的感染过程中关键的早期步骤。
The cystic fibrosis transmembrane conductance regulator (CFTR) protein is an epithelial receptor mediating the translocation of Salmonella enterica serovar Typhi to the gastric submucosa. Since the level of cell surface CFTR is directly related to the efficiency of serovar Typhi translocation, the goal of this study was to measure CFTR expression by the intestinal epithelium during infection. CFTR protein initially present in the epithelial cell cytoplasm was rapidly trafficked to the plasma membrane following exposure to live serovar Typhi or bacterial extracts. CFTR-dependent bacterial uptake by epithelial cells increased (>100-fold) following CFTR redistribution. The bacterial factor which triggers CFTR redistribution is heat and protease sensitive. These data suggest that serovar Typhi induces intestinal epithelial cells to increase membrane CFTR levels, leading to enhanced bacterial ingestion and submucosal translocation. This could be a key, early step in the infectious process leading to typhoid fever.