PRJNA422303
Immune response of Atlantic salmon against to Piscirickettsia salmonis
Piscirickettsiosis is the main bacterial disease affecting the Chilean salmon farming industry and is responsible for high economic losses. The development of effective strategies to control piscirickettsiosis has been limited in part by insufficient knowledge of the host response. The aim of this study was to use RNA sequencing to describe the transcriptional profile of the response of post-smolt Atlantic salmon infected by LF-89-like or EM-90-like Piscirickettsia salmonis. Enrichment and pathway analyses of the differentially expressed genes revealed several central signatures following infection. These included the positive regulation of DC-SIGN and TLR5 signaling, which converge at the NF-?B level to modulate the response of proinflammatory cytokines, particularly in PS-EM-90-infected fish. P. salmonis induced a IFN-inducible response (e.g IRF-1 and GBP-1), but inhibited the humoral and cell-mediated immune responses. P. salmonis induced a significant cytoskeletal reorganization, but decreased lysosomal protease activity and caused the degradation of proteins associated with cellular stress. Infection with these isolates also delayed protein transport, antigen processing, vesicle trafficking and autophagy. Both P. salmonis isolates promoted cell survival and proliferation and inhibited apoptosis. Both groups of Trojan fish showed similar pathways to modulate the immune response at 5 dpi, but the transcriptomic profile in the head kidney of the cohabitants fish infected by PS-LF-89 and PS-MS-90 at day 35 after the infection of the Trojan fish was relatively different, probably associated with the different degree of pathogenicity each isolate. Our study showed the most important biological mechanisms used by P. salmonis, regardless of the isolate, to evade the immune response, maintain the viability of host cells, increase intracellular replication and persistence at the infection site. These results improve the understanding of the mechanisms by which P. salmonis interacts with its host and may serve as a basis for the development of effective strategies for the control of piscirickettsiosis.