Project description:Fish in aquaculture farms frequently face unfavarouble husbandry conditions and other unpredictable situations, which are sometimes part of routine procedures. However, managing stress originated from these situations is crucial to ensure the sustainability of the production. When fish is exposed to prolonged stress, and overload of the physiological systems can occur and the fish may no longer be able to adapt and restore homeostasis, and this can impair the animal performance, such as growth and immunity, and consequently fish welfare. In this study the genes and gene families responsible for the molecular stress response to different challenges in gilthead seabream was assessed. Gilthead seabream adults were exposed to overcrowding, net-handling and hypoxia, in separate trials, each against a control group. Overcrowding and net-handling trials lasted for a month and half (chronic stress) and hypoxia for 48h (acute stress). The liver was the chosen organ for this transcriptomics analysis as this plays a crucial role in stress adaptation. The characterization of stress adaptation mechanisms provides valuable knowledge for the future selective breeding of more resilient commercial species that can thrive under changing conditions and adapt well to life in captivity, while ensuring high welfare standards.
Project description:As tissue macrophages of the central nervous system (CNS), microglia are critically involved in diseases of the CNS. However, it remains unknown what controls their maturation and activation under homeostatic conditions. Here we reveal significant contributions of the host microbiota to microglia homeostasis as germ-free (GF) mice displayed global defects in microglia with altered cell proportions and an immature phenotype leading to impaired innate immune responses. Temporal eradication of host microbiota severely changed microglia properties. Limited microbiota complexity also resulted in defective microglia. In contrast, recolonization with a complex microbiota partially restored microglia features. We determined that short-chain fatty acids (SCFA), microbiota-derived bacterial fermentation products, regulate microglia homeostasis. Accordingly, mice deficient for the SCFA receptor FFAR2 mirrored microglia defects found under GF conditions. These findings reveal that host bacteria vitally regulate microglia maturation and function, whereas microglia impairment can be restored to some extent by complex microbiota. For acute inflammatory challenges, LPS was applied intracranially and 6 hours later, animals were analyzed. Control animals were injected PBS i.c. Transcriptional profiles of FACS-sorted microglia were assessed using Affymetrix® (Santa Clara, USA) GeneChip Arrays (Mouse Gene 2.1 ST Arrays).
Project description:As tissue macrophages of the central nervous system (CNS), microglia are critically involved in diseases of the CNS. However, it remains unknown what controls their maturation and activation under homeostatic conditions. Here we reveal significant contributions of the host microbiota to microglia homeostasis as germ-free (GF) mice displayed global defects in microglia with altered cell proportions and an immature phenotype leading to impaired innate immune responses. Temporal eradication of host microbiota severely changed microglia properties. Limited microbiota complexity also resulted in defective microglia. In contrast, recolonization with a complex microbiota partially restored microglia features. We determined that short-chain fatty acids (SCFA), microbiota-derived bacterial fermentation products, regulate microglia homeostasis. Accordingly, mice deficient for the SCFA receptor FFAR2 mirrored microglia defects found under GF conditions. These findings reveal that host bacteria vitally regulate microglia maturation and function, whereas microglia impairment can be restored to some extent by complex microbiota.