IFN-γ Manipulates NOD1-Mediated Interaction of Autophagy and <i>Edwardsiella piscicida</i> to Augment Intracellular Clearance in Fish

Abstract Edwardsiella piscicida is an intracellular pathogenic bacterium accounting for significant losses in farmed fish. Currently, cellular and molecular mechanisms underlying E. piscicida–host cross-talk remain obscure. In this study, we revealed that could increase microtubule-associated protein L chain 3 (LC3) puncta grass carp (Ctenopharyngodon idella) monocytes/macrophages a cell line, Epithelioma papulosum cyprini. The autophagic response was confirmed by detecting the colocalization of with LC3-positive autophagosomes LysoTracker-probed lysosomes cells. Moreover, unveiled machinery targeting which nucleotide-binding oligomerization domain receptor 1 (NOD1) functioned as sensor to interact recruit autophagy-related gene (ATG) 16L1 bacteria. Meanwhile, decreased mRNA levels NOD1 ATG16L1 estrogen-related receptor-α–dependent manner, suggesting possible mechanism escaping autophagy. Subsequently, examined effects various virulence factors on expression found two them, EVPC ESCB, reduce via ubiquitin-dependent proteasomal degradation. Furthermore, intrinsic regulator IFN-γ enhance or autophagosomes, its involvement interaction between autophagy piscicida. Along short-time treatment caused clearance through autophagy-dependent mechanism. Collectively, our works demonstrated NOD1-mediated autophagy–E. dialogues uncovered involving against bacteria