Trained Immunity Provides Long-Term Protection against Bacterial Infections in Channel Catfish

Abstract

Beta glucan exposure induced trained immunity in channel catfish that conferred long-term protection against Edwardsiella ictaluri and Edwardsiella piscicida infections one month post exposure. Flow cytometric analyses demonstrated that isolated macrophages and neutrophils phagocytosed higher amounts of E. ictaluri and E. piscicida. Beta glucan induced changes in the distribution of histone modifications in the monomethylation and trimethylation of H3K4 and modifications in the acetylation and trimethylation of H3K27. KEGG pathway analyses revealed that these modifications affected expressions of genes controlling phagocytosis, phagosome functions and enhanced immune cell signaling. These analyses correlate the histone modifications with gene functions and to the observed enhanced phagocytosis and to the increased survival following bacterial challenge in channel catfish. These data suggest the chromatin reconfiguration that directs trained immunity as demonstrated in mammals also occurs in channel catfish. Understanding the mechanisms underlying trained immunity can help us design prophylactic and non-antibiotic based therapies and develop broad-based vaccines to limit bacterial disease outbreaks in catfish production.

Progress and perspective of trained immunity in teleost fish

“…Likewise, in channel catfish ( Ictalurus punctatus ), β‐glucan exposure could induce trained immunity and confer long‐term heterologous protection against bacterial infections with Edwardsiella ictaluri and Edwardsiella piscicida , as long as 1 month post‐exposure 75 . In this study, specifically, Petrie‐Hanson et al did analyse epigenetic changes in the distribution of histone modifications in monomethylation and trimethylation of H3K4, and detected modifications in the acetylation and trimethylation of H3K27.…”

“…Likewise, in channel catfish (Ictalurus punctatus), β-glucan exposure could induce trained immunity and confer long-term heterologous protection against bacterial infections with Edwardsiella ictaluri and Edwardsiella piscicida, as long as 1 month post-exposure. 75 In this study, specifically, Petrie-Hanson et al did analyse epigenetic changes in the distribution of histone modifications in monomethylation and trimethylation of H3K4, and detected modifications in the acetylation and trimethylation of H3K27. Indeed, they suggested that chromatin reconfiguration might direct trained immunity similar to what has been identified for mammals 75 ; however, the type of effector cells, how these epigenetic changes would affect these effector cells, and their direct association with β-glucan induced trained immunity remain to be elucidated.…”

“…1 However, according to the new concept, trained innate immune cells might result in longer-term protection that lasts for several days, weeks or even months. 3,7,12,75,76 Although previous concepts preferred the term 'memory' to be reserved for lymphocytes and adaptive immune responses, 77 there is no clear-cut point in time that would unambiguously define the moment when priming becomes training. Probably this criterion for distinguishing between them is related to longer-term epigenetic changes, which were primarily associated with training.…”

“…Classically, the studies on innate immune cells have shaped our ideas on the role of innate immunity, which were linked to the activation of cells for a few days only 1 . However, according to the new concept, trained innate immune cells might result in longer‐term protection that lasts for several days, weeks or even months 3,7,12,75,76 . Although previous concepts preferred the term ‘memory’ to be reserved for lymphocytes and adaptive immune responses, 77 there is no clear‐cut point in time that would unambiguously define the moment when priming becomes training.…”