Abstract
BackgroundThe salmon louse (Lepeophtheirus salmonis Krøyer), an ectoparasitic copepod with a complex life cycle causes significant losses in salmon aquaculture. Pesticide treatments against the parasite raise environmental concerns and their efficacy is gradually decreasing. Improvement of fish resistance to lice, through biological control methods, needs better understanding of the protective mechanisms. We used a 21 k oligonucleotide microarray and RT-qPCR to examine the time-course of immune gene expression changes in salmon skin, spleen, and head kidney during the first 15 days after challenge, which encompassed the copepod and chalimus stages of lice development.ResultsLarge scale and highly complex transcriptome responses were found already one day after infection (dpi). Many genes showed bi-phasic expression profiles with abrupt changes between 5 and 10 dpi (the copepod-chalimus transitions); the greatest fluctuations (up- and down-regulation) were seen in a large group of secretory splenic proteases with unknown roles. Rapid sensing was witnessed with induction of genes involved in innate immunity including lectins and enzymes of eicosanoid metabolism in skin and acute phase proteins in spleen. Transient (1-5 dpi) increase of T-cell receptor alpha, CD4-1, and possible regulators of lymphocyte differentiation suggested recruitment of T-cells of unidentified lineage to the skin. After 5 dpi the magnitude of transcriptomic responses decreased markedly in skin. Up-regulation of matrix metalloproteinases in all studied organs suggested establishment of a chronic inflammatory status. Up-regulation of putative lymphocyte G0/G1 switch proteins in spleen at 5 dpi, immunoglobulins at 15 dpi; and increase of IgM and IgT transcripts in skin indicated an onset of adaptive humoral immune responses, whereas MHCI appeared to be down-regulated.ConclusionsAtlantic salmon develops rapid local and systemic reactions to L. salmonis, which, however, do not result in substantial level of protection. The dramatic changes observed after 5 dpi can be associated with metamorphosis of copepod, immune modulation by the parasite, or transition from innate to adaptive immune responses.
Highlights
The salmon louse (Lepeophtheirus salmonis Krøyer), an ectoparasitic copepod with a complex life cycle causes significant losses in salmon aquaculture
Lice count and a summary of gene expression changes The number of lice was determined at 15 dpi, and high counts (58.4 ± 9.48 lice per fish, all at chalimus I to III stage) from 100 copepodids per fish of initial infection confirmed the lack of Atlantic salmon’s ability to clear the parasite
Given low redundancy of the platform, these numbers are close to numbers of differentially expressed genes (DEG)
Summary
The salmon louse (Lepeophtheirus salmonis Krøyer), an ectoparasitic copepod with a complex life cycle causes significant losses in salmon aquaculture. The salmon louse (Lepeophtheirus salmonis Krøyer) is a widespread disease-causing marine ectoparasitic copepod infecting wild and farmed salmonids. The development of L. salmonis encompasses ten stages: two nauplii, a copepodid, four chalimus, two pre-adult, and by a frontal filament. Even though an increase in virulence by L. salmonis has been observed as the parasite reaches the pre-adult stages [2], the chalimus stage can account for smolt mortalities (e.g. in small pink salmon [3]). Lice originating from farmed salmon may cause infections and mortality on wild salmonids [4,5]
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