Introduction
Skin ulceration is a persistent issue in Norwegian salmon farming, adversely affecting fish welfare, increasing mortality rates, and diminishing product quality. The primary causes of skin ulcer formation are mechanical handling and bacterial infections, with winter ulcer disease caused by Moritella viscosa being particularly problematic in Northern Norway. The skin, composed of layers such as mucus, epidermis, dermis, and hypodermis, acts as the first line of defense against environmental changes, physical damage, and infections. Understanding the responses triggered in these skin layers is crucial for developing effective strategies to enhance fish health and resilience against environmental stressors and infections.
Materials and methods
Direct exposure of scale explants (SE) from Atlantic salmon of various sizes to marine commensal bacteria of the skin, as well as the skin pathogens M. viscosa and Tenacibaculum finnmarkense , has been utilized to investigate initial bacterial-skin interaction responses. Additionally, a full commercial-scale Atlantic salmon feeding trial was conducted under Arctic conditions, testing different levels and sources of dietary lipids. The fish were fed one of three diets: 7.5% or 10% of the fatty acids (FA) as EPA and DHA from fish oil, or 10% of the FA as EPA and DHA from a combination of 5% fish oil and 5% algae oil, each in triplicate net-pens. All three diets were designed to meet the known nutritional requirements of Atlantic salmon. Data from the end of the production cycle at slaughter will be presented to demonstrate dietary effects on skin, including SE to examine lipid impacts on M. viscosa responses. Gene expression analysis was performed using microarray, cell morphology, stress and migration capacity was assessed using imaging and immunocytochemical detection , and skin health and characteristics evaluated for a more comprehensive understanding of the initial bacterial-skin interaction responses.
Results and conclusion
The SE model is a promising tool for studying skin responses. Compared to other tissue types, it has demonstrated strong immune activity with expected high expression of skin-specific genes. Direct exposure of SE to the skin pathogens M. viscosa and T. finnmarkense, consistently reproduces a panel of immune genes in Atlantic salmon across various growth stages . These responses are regulated in a dose-dependent manner. The prevalence of genes related to signaling and communication suggests that salmon scales act as sentinels, mobilizing immune responses upon bacterial encounters. Although variations are observed between bacterial species, a consistent gene set with high expression responding to bacteria has been identified. The SE model also revealed faster migration of skin cells (keratocytes), facilitating wound closure, and stimulation of genes for epithelial cell cross-linking in higher dietary lipid groups of the fish trial. Exposure to M. viscosa further enhanced immune responses in SE with higher lipid levels. This finding corroborated trial observations, where the low dietary lipid group exhibited higher mortality due to winter ulcer disease. Overall, the SE model has proven effective in advancing research on host-pathogen skin interactions.