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Pseudomonas plecoglossicida  is a temperature-dependent opportunistic pathogen which is associated with a variety of diseases in fish. During the development of “white nodules” disease, the expression of  htpG  in  P. plecoglossicida  was found to be significantly up-regulated at its virulent temperature of 18°C. The infection of  htpG -RNAi strain resulted in the onset time delay, reduction in mortality and infection symptoms in spleen of  Epinephelus coioides , and affected the bacterial tissue colonization. In order to reveal the effect of  htpG  silencing of  P. plecoglossicida  on the virulence regulation in  P. plecoglossicida  and immune response in  E. coioides , dual RNA-seq was performed and a pathogen-host integration network was constructed. Our results showed that infection induced the expression of host genes related to immune response, but attenuated the expression of bacterial virulence genes. Novel integration was found between host immune genes and bacterial virulence genes, while  IL6, IL1R2, IL1B , and  TLR5  played key roles in the network. Further analysis with GeneMANIA indicated that  flgD  and  rplF  might play key roles during the  htpG -dependent virulence regulation, which was in accordance with the reduced biofilm production, motility and virulence in  htpG -RNAi strain. Meanwhile,  IL6  and  IL1B  were found to play key roles during the defense against  P. plecoglossicida , while  CELA2, TRY, CPA1, CPA2 , and  CPB1  were important targets for  P. plecoglossicida  attacking to the host.

Dual RNA-Seq Unveils Pseudomonas plecoglossicida htpG Gene Functions During Host-Pathogen Interactions With Epinephelus coioides