Characterization of the Immune Response of Atlantic Salmon to Tenacibaculum dicentrarchi Using In Vivo and In Vitro Approaches

Tenacibaculosis, primarily caused by Tenacibaculum dicentrarchi in Chile, is now the second leading infectious cause of mortality in Chilean Atlantic salmon (Salmo salar) farming, yet the host immune response remains uncharacterized. Here, we combined in vitro and in vivo approaches to characterize the immunopathological interaction between Atlantic salmon and a Chilean T. dicentrarchi isolate. Primary head kidney macrophages stimulated with live bacteria showed early and sustained upregulation of tnfα, il1β, and il8 (4–24 h), followed by late induction of inos at 24 h, consistent with a classical M1-like proinflammatory profile. In parallel, il10 was robustly upregulated, while M2 marker arg was downregulated, reflecting balanced immunoregulation with active suppression of alternative activation. Production of TNF-α and IL-10 proteins was confirmed by immunofluorescence. An immersion challenge validated pathogenic relevance, yielding 32.4% cumulative mortality, with peak deaths at day 4 and a clinical course matching field outbreaks, including frayed fins, skin ulcers, mouth damage, and hemorrhage, with partial lesion resolution by day 28. Together, these results provide the first integrated in vitro–in vivo characterization of the Atlantic salmon response to T. dicentrarchi, combining cellular immune response profiling with experimental disease progression, and establishing a reproducible approach that captures both acute and recovery phases of disease, supporting future vaccine and therapeutic development against tenacibaculosis.