Key Laboratory of Prevention and Control of Biological Hazard Factors (Animal Origin) for Agri-food Safety and Quality, Ministry of Agriculture of China, Yangzhou University, China; Jiangsu Key Lab of Zoonosis/Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, China.
Jiangsu Key Lab of Zoonosis/Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, China; Joint International Research Laboratory of Agriculture and Agri-Product Safety, Yangzhou University, China.
Vet Microbiol. 2020 Nov;250:108867. doi: 10.1016/j.vetmic.2020.108867. Epub 2020 Sep 25.
SalmonellaPathogenicity Island 19 (SPI-19) encoded type VI secretion system (T6SS) is a virulence factor present in few serotypes of S. enterica, including S. Dublin, S. Gallinarum and S. Pullorum. Comparative genomic sequence analysis revealed that the gene clusters of SPI-19 showed high homology to T6SS2 locus from avian pathogenic Escherichia coli, implying the similar T6SS locus is potentially related to the host adaption of both pathogens. Deletion of SPI-19 in S. Pullorum caused the dramatically decreased invasion into chicken LMH epithelial cells and HD-11 macrophages, and affected survival of Salmonella within both cells. In addition, deletion of SPI-19 caused the decreased colonization of S. Pullorum in chicken liver, spleen, ileum, and cecum at the initial infection stage, and induced rapid bacterial clearance. However, the SPI-19/T6SS had no effect on bacterial killing activity and induction of cytotoxicity to HD-11 macrophages. Further analysis demonstrated SPI-19/T6SS was involved in mediating the inhibition of host Th1 and Th2 immune responses, resulting in persistent colonization of S. Pullorum in hosts.
肠炎沙门氏菌致病岛 19（SPI-19）编码的 VI 型分泌系统（T6SS）是少数肠炎沙门氏菌血清型（包括都柏林沙门氏菌、鸡沙门氏菌和鸡白痢沙门氏菌）中存在的一种毒力因子。比较基因组序列分析显示，SPI-19 的基因簇与禽致病性大肠杆菌的 T6SS2 基因座具有高度同源性，这意味着类似的 T6SS 基因座可能与两种病原体的宿主适应性有关。鸡白痢沙门氏菌中 SPI-19 的缺失导致其对鸡 LMH 上皮细胞和 HD-11 巨噬细胞的侵袭能力显著下降，并影响沙门氏菌在两种细胞内的存活。此外，SPI-19 的缺失导致鸡白痢沙门氏菌在鸡肝脏、脾脏、回肠和盲肠中的定植在初始感染阶段减少，并诱导细菌快速清除。然而，SPI-19/T6SS 对细菌杀伤活性和诱导 HD-11 巨噬细胞细胞毒性没有影响。进一步分析表明，SPI-19/T6SS 参与介导宿主 Th1 和 Th2 免疫反应的抑制，导致鸡白痢沙门氏菌在宿主中的持续定植。
