Acquired Protective Immunity in Atlantic Salmon Salmo salar against the Myxozoan Kudoa thyrsites Involves Induction of MHIIβ ⁺ CD83 ⁺ Antigen-Presenting Cells

Abstract

The histozoic myxozoan parasite causes postmortem myoliquefaction and is responsible for economic losses to salmon aquaculture in the Pacific Northwest. Despite its importance, little is known about the host-parasite relationship, including the host response to infection. The present work sought to characterize the immune response in Atlantic salmon during infection, recovery, and reexposure to After exposure to infective seawater, infected and uninfected smolts were sampled three times over 4,275 degree-days. Histological analysis revealed infection severity decreased over time in exposed fish, while in controls there was no evidence of infection. Following a secondary exposure of all fish, severity of infection in the controls was similar to that measured in exposed fish at the first sampling time but was significantly reduced in reexposed fish, suggesting the acquisition of protective immunity. Using immunohistochemistry, we detected a population of MHIIβ cells in infected muscle that followed a pattern of abundance concordant with parasite prevalence. Infiltration of these cells into infected myocytes preceded destruction of the plasmodium and dissemination of myxospores. Dual labeling indicated a majority of these cells were CD83/MHIIβ Using reverse transcription-quantitative PCR, we detected significant induction of cellular effectors, including macrophage/dendritic cells (//), B cells (/), and cytotoxic T cells (/), in the musculature of infected fish. These data support a role for cellular effectors such as antigen-presenting cells (monocyte/macrophage and dendritic cells) along with B and T cells in the acquired protective immune response of Atlantic salmon against .

Acquired protective immune response in a fish-myxozoan model encompasses specific antibodies and inflammation resolution

“…In regard to myxozoan infections, in rainbow trout re-exposed to T. bryosalmonae, the cellular adaptive response (increase in IgM + circulating B cells) resulted in lower prevalence and intensity of infection [44]. In Atlantic salmon re-exposed to K. thyrsites the cell-mediated immune response by means of macrophages/dendritic cells, cytotoxic T cells, and B cells, resulted in lower parasite prevalence and infection intensity [43].…”

“…scophthalmi in turbot [42]. The severity of infection with K. thyrsites was decreased in re-exposed Atlantic salmon, which exhibited an acquired protective immune response mounted on antigen-presenting monocyte/macrophage and dendritic cells, along with B and T cells in the muscle tissue [43]. Rainbow trout re-exposed to T. bryosalmonae developed immune protection through the increase of circulating IgM + B cells and upregulated mRNA levels of secretory IgM in the posterior kidney [44].…”

“…Cytotoxic activity, mainly related to CD8 + CTLs, was also linked to successful resolution of infection and protection upon re-exposure in Atlantic salmon infected with the myxozoan parasite K. thyrsites [43].…”

Hints on T cell responses in a fish-parasite model: Enteromyxum leei induces differential expression of T cell signature molecules depending on the organ and the infection status

“…Thus, we hypothesize that fish with more CD8 + cells or with higher levels of activation of this subtype have more chances to successfully avoid or clear the infection. A recent study in Atlantic salmon ( Salmo salar ) infected with the myxozoan Kudoa thyrsites showed that CTLs are key for resolution of infection and protection against reinfection [ 67 ].…”

Water temperature, time of exposure and population density are key parameters in Enteromyxum leei fish‐to‐fish experimental transmission

“…Parasite load can be measured in degree days, which are correlated with the time that the fish have been exposed to infective stages of the parasite and the temperature during this period (Braden et al, ; Jones & Long, ; Thompson, Snekvik, & Vincent, ). These infective stages can be either spores from the definitive invertebrate host (Feist, Longshaw, Canning, & Okamura, ; Markiw, ) or proliferative stages from already infected fishes (de Buron et al, ; Estensoro et al, ).…”