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Integrative Study of Physiological Changes Associated with Bacterial Infection in Pacific Oyster Larvae

Figure 4

Schematic diagrams of physiological changes induced during bacterial infection in C. gigas larvae.

Infection impact on larval physiology was investigated through immunity (1), cellular stress (2), energetic metabolism (3) and lipid metabolism (4) using physiological, enzymatic, biochemical and molecular analysis. Results suggest that bacterial infection induce the activation of the immune response (non-self recognition (1a), NF-κB signaling pathway (1b), haematopoiesis (1d), synthesis of inhibitor of metalloproteinase, antimicrobial peptide (1c) and phagocytosis (1e) allowing the destruction of pathogenic bacteria. The production of reactive oxygen species (ROS) during the phagocytosis process was managed by antioxidant defenses (2a) and cytoprotective proteins (2b). Infection affects the feeding activity (3a) which change the energy status of larvae (decline of metabolic rate (3b), energy reserve consumption (3c), β-oxidation activation (3d) and lower lipids storage (3e)). Besides metabolic changes, fatty acid remodeling in polar lipids (4a) is associated to pathogen exposure, as suggested by changes in phosphatidylinositol and lysophosphatidylcholine composition, non-methylene–interrupted fatty acids accumulation, lower content of major C20 polyunsaturated fatty acids and activation of desaturases. Finally, infection induces the activation of phospholipase and lipoxygenase (4b) probably through NF-κB regulation (4c) to initiate eicosanoïdes and lysophosphatidic acid (LPA) pathways. See discussion for details.

Figure 4