The bacterium Piscirickettsia salmonis is the etiological agent of salmonid rickettsial septicemia (SRS), a severe disease that causes major economic losses to the Atlantic salmon aquaculture industry every year. Little is known about the infective strategy of P. salmonis, which is able to infect, survive within, and replicate inside salmonid macrophages as an intracellular parasite. Similarly there is little knowledge concerning the fish host's response to invasion by this pathogen. We have examined the transcriptional response of postsmolt Atlantic salmon (Salmo salar) to P. salmonis at 48 h following infection in three tissues, liver, head kidney, and muscle, using an Atlantic salmon oligonucleotide microarray (Salar_2, Agilent 4x44K). The infection led to a large alteration of transcriptional activity in all the tissues studied. In infected salmon 886, 207, and 153 transcripts were differentially expressed in liver, head kidney, and muscle, respectively. Assessment of enrichment for particular biological pathways by gene ontology analysis showed an upregulation of genes involved in oxidative and inflammatory responses in infected fish, indicative of the activation of the innate immune response. The downregulation of genes involved in the adaptive immune response, G protein signaling pathway, and apoptotic process in infected fish may be reflective of mechanisms used by P. salmonis to survive, replicate, and escape host defenses. There was also evidence of differential responses between studied tissues, with protein metabolism being decreased in muscle of infected fish and with a concomitant increase being shown in liver.
|Number of pages||14|
|Publication status||Published - 1 Nov 2011|
- salmonid rickettsial septicemia