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.