Project description:Bacterial pathogen Moritella viscosa, the causative agent of winter ulcer, causes heavy losses in Atlantic salmon aquaculture. The study compared responses in salmon reared under normal condition (G100) and fish exposed to hypoxia - 60% saturation of dissolved oxygen - at early life (G60). G60 showed lower survival after challenge. Analyses were performed in the most affected tissues: skin and spleen
Project description:Norway is the largest producer and exporter of farmed Atlantic salmon (Salmo salar) worldwide. Skin disorders correlated with bacterial infections represent an important challenge for fish farmers due to the economic losses caused. Little is known about this topic, thus studying the skin-mucus of Salmo salar and its bacterial community depict a step forward in understanding fish welfare in aquaculture. In this study, we used label free quantitative mass spectrometry to investigate the skin-mucus proteins associated with both Atlantic salmon and bacteria. In addition, the microbial temporal proteome dynamics during 9 days of mucus incubation with sterilized seawater was investigated, in order to evaluate their capacity to utilize mucus components for growth in this environment.
Project description:Fish skin is a critical regulatory organ, serving not only as a physical barrier to pathogen entry, but also as a sophisticated integrator of aquatic environmental, social and nutritional cues through roles in immunity, osmoregulation, and endocrine signaling. Integral to the complexity of teleost skin is the mucus layer secreted by epidermal goblet cells. Pathogen invasion can disrupt this delicate homeostasis with profound impacts on signaling throughout the organism. Here, we investigated the transcriptional effects of virulent A. hydrophila infection in blue catfish skin, Ictalurus furcatus. We utilized an 8X60K Agilent microarray to examine gene expression profiles at critical early timepoints following challenge—2 h, 12 h, and 24 h. Expression of a total of 1,155 unique genes was significantly perturbed during at least one timepoint. We observed dysregulation of a number of genes involved in including antioxidant/apoptosis, cytoskeletal rearrangement, immune response, junctional/adhesion, and proteases. In particular, A. hydrophila infection rapidly altered a number potentially critical lectins, chemokines, interleukins, and other mucosal factors in a manner predicted to enhance its ability to adhere and invade the catfish host. Two-condition experiment, control vs. infected skin. Biological replicates: 3 control replicates, 3 infected replicates.3 timepoints
Project description:Swift recruitment of phagocytic leukocytes is critical to prevent infection when bacteria breach through the protective layers of the skin. According to canonical models, this occurs via an indirect process that is initiated by contact of bacteria with resident skin cells and which is independent of the pathogenic potential of the invader. Here, we describe a more rapid mechanism of leukocyte recruitment to the site of intrusion of the important skin pathogen Staphylococcus aureus that is based on direct recognition of specific bacterial toxins, the phenol-soluble modulins (PSMs), by circulating leukocytes. This early recruitment was dependent on the transcription factor EGR1 and significantly contributed to the prevention of infection. Our findings refine the classical notion of the non-specific and resident cell-dependent character of the innate immune response to bacterial infection by demonstrating a pathogen-specific high-alert mechanism involving direct recruitment of immune effector cells by secreted bacterial products.
Project description:Tenacibaculum finnmarkense is a novel Gram-negative, aerobic bacterial strain causing skin ulcers in Atlantic salmon. This is an emerging pathogen, which may cause serious problems to aquaculture. The study was designed to compare the life stages (smolt and posmolt) and to assess effects of environment (fresh and brackis water) on the course of disease and salmon responses to the pathogen.