The effect of acute heat stress on the Chinook salmon immune system and their ability to combat Vibrio anguillarum infection and mortality.

The frequency, duration, and intensity of heatwaves in western Canada is expected to rise in the coming years, and as a result, shallow streams will also experience drastic temperature fluctuations. This poses a problem for salmonids as encountering high water temperatures may increase their susceptibility to infectious disease. An environmentally applicable mock heat shock was performed on juvenile Chinook salmon and their immunological responses were measured for 14 days afterwards. Chinook salmon also received an injection of live Vibrio anguillarum after heat shock to determine if heat rendered them immunocompromised to systemic bacterial infection. il1b, il8, tnfa, il10, tgfb, hsp47, hsp70, and hsp90 transcripts were quantified by qPCR in the spleen, gills, and hindgut. Heat shock did not affect mortality rates due to vibriosis compared to controls. Additionally, heat shock mitigated the pro-inflammatory and anti-inflammatory responses needed to combat infection by initially upregulating il1b, tnfa, il8, and il10, then returning to control levels by three days post-infection. Transcripts of hsp47 and hsp90 were upregulated in response to both heat shock and V. anguillarum. This research reports the first HSP47 protein measurements in Chinook salmon in plasma, which did not differ between any treatment groups. Plasma cortisol and lactate concentrations significantly increased, then returned to basal levels 6-h post-heat shock. Altogether, these data indicate that the experimental heat shock had a positive preconditioning effect on Chinook salmon and provides new insights on the interactions between the host, environment, and pathogen over a 14-day period.