Stress Impairs Skin Barrier Function and Induces α2-3 Linked N-Acetylneuraminic Acid and Core 1 O-Glycans on Skin Mucins in Atlantic Salmon, Salmo salar.

The skin barrier consists of mucus, primarily comprising highly glycosylated mucins, and the epithelium. Host mucin glycosylation governs interactions with pathogens and stress is associated with impaired epithelial barrier function. We characterized Atlantic salmon skin barrier function during chronic stress (high density) and mucin O-glycosylation changes in response to acute and chronic stress. Fish held at low (LD: 14-30 kg/m3) and high densities (HD: 50-80 kg/m3) were subjected to acute stress 24 h before sampling at 17 and 21 weeks after start of the experiment. Blood parameters indicated primary and secondary stress responses at both sampling points. At the second sampling, skin barrier function towards molecules was reduced in the HD compared to the LD group (Papp mannitol; p < 0.01). Liquid chromatography-mass spectrometry revealed 81 O-glycan structures from the skin. Fish subjected to both chronic and acute stress had an increased proportion of large O-glycan structures. Overall, four of the O-glycan changes have potential as indicators of stress, especially for the combined chronic and acute stress. Stress thus impairs skin barrier function and induces glycosylation changes, which have potential to both affect interactions with pathogens and serve as stress indicators.

Modelling growth performance and feeding behaviour of Atlantic salmon (Salmo salar L.) in commercial-size aquaculture net pens: Model details and validation through full-scale experiments.

We have developed a mathematical model which estimates the growth performance of Atlantic salmon in aquaculture production units. The model consists of sub-models estimating the behaviour and energetics of the fish, the distribution of feed pellets, and the abiotic conditions in the water column. A field experiment where three full-scale cages stocked with 120,000 salmon each (initial mean weight 72.1  ± SD 2.8 g) were monitored over six months was used to validate the model. The model was set up to simulate fish growth for all the three cages using the feeding regimes and observed environmental data as input, and simulation results were compared with the experimental data. Experimental fish achieved end weights of 878, 849 and 739 g in the three cages respectively. However, the fish contracted Pancreas Disease (PD) midway through the experiment, a factor which is expected to impair growth and increase mortality rate. The model was found able to predict growth rates for the initial period when the fish appeared to be healthy. Since the effects of PD on fish performance are not modelled, growth rates were overestimated during the most severe disease period. This work illustrates how models can be powerful tools for predicting the performance of salmon in commercial production, and also imply their potential for predicting differences between commercial scale and smaller experimental scales. Furthermore, such models could be tools for early detection of disease outbreaks, as seen in the deviations between model and observations caused by the PD outbreak. A model could potentially also give indications on how the growth performance of the fish will suffer during such outbreaks. STATEMENT OF RELEVANCE: We believe that our manuscript is relevant for the aquaculture industry as it examines the growth performance of salmon in a fish farm in detail at a scale, both in terms of number of fish and in terms of duration, that is higher than usual for such studies. In addition, the fish contracted a disease (PD) midway through the experiment, thus resulting in a detailed dataset containing information on how PD affects salmon growth, which can serve as a foundation to understanding disease effects better. Furthermore, the manuscript describes an integrated mathematical model that is able to predict fish behaviour, growth and energetics of salmon in response to commercial production conditions, including a dynamic model of the distribution of feed pellets in the production volume. To our knowledge, there exist no models aspiring to estimate such a broad spectre of the dynamics in commercial aquaculture production cages. We believe this model could serve as a future tool to predict the dynamics in commercial aquaculture net pens, and that it could represent a building block that can be utilised in a future development of knowledge-driven decision-support tools for the salmon industry.

Molecular and physiological responses to long-term sublethal ammonia exposure in Atlantic salmon (Salmo salar).

The objective of this study was to determine the underlying physiological and molecular responses to long-term sublethal ammonia exposure in Atlantic salmon (Salmo salar) parr. Previous studies have predominately focused on mechanisms during acute, short-term exposure. For that purpose Atlantic salmon parr were exposed to four ammonia concentrations between 4 and 1800 µmol l(-1) total ammonia nitrogen (TAN), and subjected to two feeding regimes for 15 weeks. Elevated environmental ammonia and full feeding strength caused an initial increase in plasma ammonia levels ([T(amm)]) after 22 days of exposure, which thereafter declined and remained similar to the control animals towards the end of the study. On the other hand, a progressive decrease in plasma urea levels was evident throughout the entire exposure period and depended on the concentration of environmental ammonia, with the largest decrease in urea levels observed at the highest ammonia concentrations (1700 and 1800 µmol l(-1) TAN). We hypothesized that the successful adaptation to long-term elevated ammonia levels would involve an increased capacity for carrier-facilitated branchial excretion. This hypothesis was strengthened by the first evidence of an up-regulation of branchial transcription of the genes encoding the Rhesus (Rh) glycoproteins, Rhcg1 and Rhcg2, urea transporter (UT) and aquaporin 3a (Aqp3a), during long-term exposure. Of the Rhesus glycoprotein (Rh) mRNAs, Rhcg1 was up-regulated at all tested ammonia levels, while Rhcg2 showed a concentration-sensitive increase. Increased transcription levels of V-type H(+)-ATPase (H(+)-ATPase) were observed at the highest ammonia concentrations (1700 and 1800 µmol l(-1) TAN) and coincided with an up-regulation of Rhcg2 at these concentrations. Transcription of UT and Aqp3a was increased after 15 weeks of exposure to low ammonia levels (470 and 480 µmol l(-1) TAN). A significant increase in brain glutamine (Gln) concentration was observed for full fed Atlantic salmon after 22 days and in fish with restricted feeding after 105 days of exposure to 1800 and 1700 µmol l(-1) TAN, respectively, without any concomitant decrease in brain glutamate (Glu) concentrations. These results suggest that Gln synthesis is an ammonia detoxifying strategy employed in the brain of Atlantic salmon parr during long-term sublethal ammonia exposure. Full feed strength had an additive effect on plasma [T(amm)], while the restricted feeding regime postponed the majority of the observed physiological and molecular responses. In conclusion, Atlantic salmon parr adapts to the long-term sublethal ammonia concentrations with increased branchial transcription levels of ammonia and urea transporting proteins and ammonia detoxification in the brain.