Abstract
In the present study, Larimichthys crocea and Pseudomonas plecoglossicida were selected as a host-pathogen interaction model for teleosts and prokaryotic pathogens. Five shRNAs were designed and synthesized to silence the fliA gene, all of which resulted in pronounced reductions in fliA mRNA; the mutant strain with the best silencing efficiency of 92.16% was chosen for subsequent analysis. A significant decrease in motility, intracellular survival and escape was observed for the fliA-RNAi strain of P. plecoglossicida, whereby silencing of the fliA gene led to a 30% decrease in mortality and a four-day delay in the onset of infection in L. crocea. Moreover, silencing of P. plecoglossicida fliA resulted in a significant change in both the pathogen and host transcriptome in the spleens of infected L. crocea. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of pathogen transcriptome data showed that silencing fliA resulted in downregulation of 18 flagellum-related genes; KEGG analysis of host transcriptome data revealed that infection with the fliA-RNAi strain caused upregulation of 47 and downregulation of 106 immune-related genes. These pathogen-host interactions might facilitate clearance of P. plecoglossicida by L. crocea, with a significant decrease in fliA-RNAi P. plecoglossicida strain virulence in L. crocea.
Highlights
Flagella are an important structure in bacteria and are widely recognized to be involved in their pathogenesis [1,2]
Knocking out fliA in P. aeruginosa resulted in reduced motility, with decreased colonization in the intestines of mice because flagella were not synthesized [19]
The results indicate that fliA plays a critical role in flagellar assembly, especially in the host
Summary
Flagella are an important structure in bacteria and are widely recognized to be involved in their pathogenesis [1,2]. More than 50 genes are involved in the synthesis of flagella, and they are expressed in a strictly regulated and hierarchical manner [11]. Knocking out fliA in P. aeruginosa resulted in reduced motility, with decreased colonization in the intestines. Σ28 has been documented to regulate flagellar synthesis in Escherichia coli [14], Campylobacter jejuni [15], Pseudomonas aeruginosa [16], Salmonella typhimurium [17] and Vibrio cholera [18]. Knocking out fliA in P. aeruginosa resulted in reduced motility, with decreased colonization in the intestines of mice because flagella were not synthesized [19].
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