The SPI-19 encoded T6SS is required for Salmonella Pullorum survival within avian macrophages and initial colonization in chicken dependent on inhibition of host immune response

•The SPI-19 from S. Pullorum displays high homology to T6SS2 in APEC.•SPI-19/T6SS is required for S. Pullorum invasion and survival within avian epithelial cells and macrophages.•SPI-19/T6SS contributes to initial colonization of S. Pullorum in chicken organs and intestinal tissues.•SPI-19/T6SS inhi...

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Published in:Veterinary microbiology 2020-11, Vol.250, p.108867-108867, Article 108867
Main Authors: Xian, Honghong, Yuan, Yu, Yin, Chao, Wang, Zhenyu, Ji, Ruoyun, Chu, Chao, Jiao, Xinan, Li, Qiuchun
Format: Article
Language:English
Subjects:
Cecum
Clonal deletion
Colonization
Cytotoxicity
Epithelial cells
Gene clusters
Gene deletion
Genomic analysis
Genomics
Homology
Ileum
Immune clearance
Immune response
Lymphocytes T
Macrophages
Salmonella
Salmonella entericaserovar Pullorum (S. Pullorum)
Sequence analysis
Serotypes
SPI-19
Spleen
T6SS
Virulence factors
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Summary:•The SPI-19 from S. Pullorum displays high homology to T6SS2 in APEC.•SPI-19/T6SS is required for S. Pullorum invasion and survival within avian epithelial cells and macrophages.•SPI-19/T6SS contributes to initial colonization of S. Pullorum in chicken organs and intestinal tissues.•SPI-19/T6SS inhibits host Th1/Th2 immune responses to enable persistent infection of S. Pullorum in chickens. 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.
ISSN:0378-1135
1873-2542
DOI:10.1016/j.vetmic.2020.108867