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首页> 外文期刊>Microbial Pathogenesis >Type IVB pili are required for invasion but not for adhesion of Salmonella enterica serovar Typhi into BHK epithelial cells in a cystic fibrosis transmembrane conductance regulator-independent manner.
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Type IVB pili are required for invasion but not for adhesion of Salmonella enterica serovar Typhi into BHK epithelial cells in a cystic fibrosis transmembrane conductance regulator-independent manner.

机译:IV型 B 菌毛是侵袭性必需的,而肠沙门氏菌血清型伤寒菌则不需要囊性纤维化跨膜电导调节剂,而只能粘附在BHK上皮细胞中。

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摘要

The cystic fibrosis transmembrane conductance regulator (CFTR) has been proposed as an epithelial cell receptor for the entry of Salmonella Typhi but not Salmonella Typhimurium. The bacterial ligand recognized by CFTR is thought to reside either in the S. Typhi lipopolysaccharide core region or in the type IV pili. Here, we assessed the ability of virulent strains of S. Typhi and S. Typhimurium to adhere to and invade BHK epithelial cells expressing either the wild-type CFTR protein or the DeltaF508 CFTR mutant. Both S. Typhi and S. Typhimurium invaded the epithelial cells in a CFTR-independent fashion. Furthermore and also in a CFTR-independent manner, a S. Typhi pilS mutant adhered normally to BHK cells but displayed a 50% reduction in invasion as compared to wild-type bacteria. Immunofluorescence microscopy revealed that bacteria and CFTR do not colocalize at the epithelial cell surface. Together, our results strongly argue against the established dogma that CFTR is a receptor for entry of Salmonella to epithelial cells.
机译:有人提出,囊性纤维化跨膜电导调节剂(CFTR)是上皮细胞受体,用于沙门氏菌伤寒沙门氏菌,但不能用于沙门氏菌鼠伤寒沙门氏菌。 CFTR识别的细菌配体被认为位于 S。 Typhi脂多糖核心区域或IV型菌毛中。在这里,我们评估了 S 毒株的能力。鼠伤寒和 S。鼠伤寒附着并侵入表达野生型CFTR蛋白或DeltaF508 CFTR突变体的BHK上皮细胞。都是 S 。 Typhi和 S 。鼠伤寒以独立于CFTR的方式侵入上皮细胞。此外,并且也以CFTR独立的方式, S。 Typhi pilS 突变体正常粘附于BHK细胞,但与野生型细菌相比,侵袭力降低了50% 。免疫荧光显微镜检查显示细菌和CFTR不在上皮细胞表面共定位。总之,我们的结果强烈反对既定的教条,即CFTR是沙门氏菌进入上皮细胞的受体。

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