| Summary: | Physical damage of tissue and multiple kinds of infections are found to cause inflammatory reactions in mammals. Regardless of the difference between non-pathogenic induced tissue damage and a bacterial infection, many of the same pathways and genes are triggered. To determine if the same phenomenon occurs in salmonid fishes, Atlantic salmon (Salmo salar) were infected with the bacteria Moritella viscosus, the causative agent of winter ulcer. The clinical signs showing visible, punctual lesions in the skin make this pathogen unique in order to study local inflammation. Muscle tissue was sampled from infected fish at 4, 7 and 14 days post infection. Samples were obtained from site of lesions and from locations without clinical signs of disease and lesions. To compare the inflammatory reactions from infected fish relative to sterile, mechanical tissue damage, rainbow trout (Oncorhynchus mykiss) were subjected to controlled tissue disruption applying sterile needles to skin and muscle tissue to one side of the fish. Samples were taken 4, 8, 24 hours and 7 days post injury from both the injured side and non injured site, internal control. From both studies, the samples were subject to real-time RT-PCR for measuring the expression of the genes IL-1β, IL-8, IL-10 and Collagen-1α. Overall, the results showed that all genes in both studies were locally induced by the infection or the injury and the expression patterns between the two models were very similar, although the kinetics were different. For both the experiments the expression of pro-inflammatory cytokines peaked first followed by an increase in the amount of IL-10 and Collagen-1α mRNA. Thus it is suggested that stimulation by pathogen associated molecular patterns (PAMPs) trigger the same genes and pathways as damage associated molecular patterns (DAMPs) in salmonid fishes.
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