Abstract

Simple SummaryThe natural presence of opportunistic pathogens in aquatic rearing systems in alignment with favorable conditions (compromised fish immune status and/or inappropriate rearing conditions) might result in serious acute disease episodes that can develop into chronic immune responses. The present study characterizes molecular, cellular and humoral markers of chronic inflammation in a fish species with high commercial value. The intense recruitment of immune cells to the inflammatory focus 21 days after triggering an immune response illustrates a clear chronic character. The cellular response was also noticed with circulating leukocyte numbers rising in the blood of the inflamed fish. Furthermore, the cellular-mediated respiratory burst peaked at 21 days post-injection, suggesting that phagocytes were still actively fighting the inflammatory agent. Regarding the molecular analysis, certain genes appear to be good markers of a chronic inflammation response due to their importance in pathways with high relevance in chronic inflammation settings. The present study can serve as a baseline to assess long-term immune-related responses in future studies.Stress-inducing husbandry and rearing conditions, bacterial infections or parasitic diseases may all lead to chronic inflammation. The immune response will then channel energy away from growth, reproduction and other important physiological processes, to fuel immune-related metabolic responses. The present study aims to unravel the mechanisms and contribute with new information on the molecular, cellular and humoral parameters of European seabass (Dicentrarchus labrax) undergoing chronic inflammation that can be used as health indicators for application in fish health management. European seabass individuals were intra-peritoneally injected with either Freund’s Incomplete Adjuvant (FIA) to induce inflammation or Hanks Balanced Salt Solution (HBSS) to serve as sham. Fish were sampled at 24 h, 7, 14 and 21 days post-injection and blood, plasma and head-kidney were collected. The results found were clear indicators of an inflamed peritoneal cavity and an ongoing systemic immune response that persisted for at least 21 days. Locally, inflammation was characterized by an intense recruitment of immune cells that was still evident 21 days after injection, thus illustrating the chronic character of the immune response. Cellular response was also noticed peripherally with leukocyte numbers rising in the blood of FIA-injected fish. Furthermore, the cellular-mediated respiratory burst peaked at 21 days post-FIA injection, suggesting that phagocytes were still actively fighting the phlogistic agent. Regarding the head-kidney molecular analysis, cxcr4 and il34 appear to be good markers of a chronic inflammation response due to their importance for pathways with high relevance in chronic inflammation settings. In addition, opioid receptor nopr seems to be a good marker of a chronic inflammation response due to its role in detecting noxious stimuli. The present study can serve as a baseline to assess long-term immune-related responses in future studies. For that, more research is nonetheless required to select more responsive and specific molecular markers.

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