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| Main Authors: | , |
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| Format: | Artículo científico |
| Language: | en |
| Published: |
Fish & shellfish immunology
2026
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| Subjects: | |
| Online Access: | https://pubmed.ncbi.nlm.nih.gov/41936922/ |
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Table of Contents:
- Edwardsiella tarda infection induces PANoptosis in gill cells of Japanese flounder Paralichthys olivaceus. Sun, Chunyan Jiang, Shuai Animals Edwardsiella tarda Enterobacteriaceae Infections Fish Diseases Gills Flatfishes Fish Proteins Cell Death Immunity, Innate Edwardsiella tarda is an important bacterial pathogen in fish aquaculture, yet the molecular mechanisms underlying infection remain largely unexplored. Here, we show that E. tarda infection induces rapid cell death in flounder gill cells in a dose- and time-dependent manner. Infected cells display severe plasma membrane disruption and loss of viability, consistent with necrotic death. Gene expression analysis revealed strong up-regulation of immune-related genes, particularly those involved in pattern recognition receptors (TLR, NLR and RIG-I) and their intracellular downstream NF-кB and MAPK signaling pathways that control inflammation and cell survival. Blocking either the NF-кB or MAPK signaling pathways markedly reduced cell death, indicating that host signaling actively contributes to infection-induced cell death. Time-lapse live-cell imaging and biochemical analyses further demonstrated that infection triggers PANoptosis, a coordinated form of lytic cell death combining pyroptosis, apoptosis, and necrosis. Inhibition of the NF-кB pathway increased expression of proinflammatory cytokines TNF-α and IL-1β, and significantly reduced bacterial burden in flounder tissues. These findings collectively reveal a previously unrecognized molecular mechanism underlying E. tarda infection-induced cell lysis, and highlight an important role of the NF-кB/MAPK signaling axis in fish inflammatory immune response and antimicrobial defense.