Early-life conditions shape baseline immune gene expression, but not pathogen-induced immune activation, in brown trout
Early-life environment and parental background can shape immune phenotypes, but whether such differences persist during infection and influence the immune response remains unclear. We used single-cell RNA sequencing to characterize kidney immune responses in brown trout (Salmo trutta) from three origins differing in parental history and early rearing: wild parents with offspring reared in the…
The background and environment in which brown trout are raised during their early life can influence their immune system's baseline gene expression, but this does not affect the immune response once they are exposed to a pathogen. Researchers utilized single-cell RNA sequencing to examine kidney immune reactions in brown trout (Salmo trutta) from three distinct origins: offspring of wild parents reared in the wild, offspring of wild parents reared in a hatchery, and offspring of hatchery parents reared in a hatchery.
Despite originating from the same river and showing no visible genetic differences, the fish exhibited noticeable disparities in gene expression, particularly within B cells. Upon exposure to Tetracapsuloides bryosalmonae, the pathogen responsible for proliferative kidney disease, the research team observed significant alterations in immune cell composition and transcriptional activity.
T cells became more abundant, while B cells, neutrophils, and proliferating progenitors exhibited the most substantial transcriptional reactions, indicating an active yet controlled response to subclinical infection. Interestingly, the marked differences in origin-related gene expression prior to infection largely dissipated in the wake of infection.
Regardless of their initial environmental or parental background, all fish eventually converged on a shared transcriptional response. Consequently, the study highlights that substantial variations in immune genes can remain undetected under resting conditions but can be overridden by pathogen exposure, ultimately leading to a common immune state.
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