Department of Veterinary Medicine, Freie Universität Berlin, Institute of Microbiology and Epizootics, Berlin, Germany.
Institute of Medical Microbiology, Rwth University Hospital Aachen, Aachen, Germany.
Gut Microbes. 2021 Jan-Dec;13(1):1973836. doi: 10.1080/19490976.2021.1973836.
pathogenicity island (SPI) 2 type three secretion system (T3SS)-mediated effector molecules facilitate bacterial survival in phagocytes but their role in the intestinal epithelium remains ill-defined. Using our neonatal murine infection model in combination with SPI2 reporter technology and RNA-Seq of sorted primary enterocytes, we demonstrate expression of SPI2 effector molecules by intraepithelial Typhimurium . Typhimurium). Contrary to expectation, immunostaining revealed that infection with SPI2 T3SS-mutants resulted in significantly enlarged intraepithelial -containing vacuoles (SCV) with altered cellular positioning, suggesting impaired apical to basolateral transmigration. Also, infection with isogenic tagged . Typhimurium strains revealed a reduced spread of intraepithelial SPI2 T3SS mutant . Typhimurium to systemic body sites. These results suggest that SPI2 T3SS effector molecules contribute to enterocyte apical to basolateral transmigration of the SCV during the early stage of the infection.
致病岛 (SPI) 2 型三型分泌系统 (T3SS) 介导的效应分子有助于细菌在吞噬细胞中存活，但它们在肠道上皮细胞中的作用仍不清楚。我们使用新生鼠感染模型，结合 SPI2 报告基因技术和分选原代肠上皮细胞的 RNA-Seq，证明 SPI2 效应分子在肠上皮内表达。鼠伤寒沙门氏菌。). 与预期相反，免疫染色显示，SPI2 T3SS 突变体感染导致含有空泡的上皮内空泡 (SCV) 显著增大，细胞位置发生改变，提示顶端到基底外侧的迁移受损。此外，用同源标记感染。鼠伤寒沙门氏菌菌株显示上皮内 SPI2 T3SS 突变体的传播减少。鼠伤寒沙门氏菌到全身身体部位。这些结果表明，SPI2 T3SS 效应分子有助于 SCV 在感染早期的肠上皮细胞顶端到基底外侧的迁移。
