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Taurine (TAU) and glutathione (GSH) have been demonstrated to have potential therapeutic efficacy against ferroptosis\u2010associated pathologies through redox modulation. However, their combined effects and underlying mechanisms in alleviating\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>A. hydrophila<\/jats:italic>\n                    <\/jats:styled-content>\n                    infection remain unclear. In this study, we investigated the protective roles of TAU, GSH and their combination in\u00a0vitro using yellow catfish (\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Pelteobagrus fulvidraco<\/jats:italic>\n                    <\/jats:styled-content>\n                    ) macrophages and grass carp (\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Ctenopharyngodon idella<\/jats:italic>\n                    <\/jats:styled-content>\n                    ) kidney (CIK) cells and in\u00a0vivo using yellow catfish challenged with\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>A. hydrophila<\/jats:italic>\n                    <\/jats:styled-content>\n                    . The results showed that TAU and GSH, either alone or in combination, alleviated oxidative stress by significantly reducing reactive oxygen species (ROS) accumulation and inhibited nuclear factor\u2010\u03baB (NF\u2010\u03baB) pathway activation. This led to downregulated expression of pro\u2010inflammatory cytokines (\n                    <jats:italic>IL\u2010<\/jats:italic>\n                    1\u03b2 and\n                    <jats:italic>TNF<\/jats:italic>\n                    \u2010\u03b1) and upregulated anti\u2010inflammatory cytokines (\n                    <jats:italic>IL\u2010<\/jats:italic>\n                    10 and\n                    <jats:italic>TGF<\/jats:italic>\n                    \u2010\u03b2), accompanied by alleviated ferroptosis. In\u00a0vivo, dietary supplementation with TAU (10 g\/kg) or GSH (350 mg\/kg) alone improved survival rates (51.7% and 38.3%, respectively), reduced tissue bacterial loads and protected intestinal and hepatic tissues by preserving mucosal barrier function. However, the TAU + GSH combination unexpectedly decreased survival (28.3%) due to excessive immunosuppression (overproduction of\n                    <jats:italic>IL\u2010<\/jats:italic>\n                    10 and\n                    <jats:italic>TGF<\/jats:italic>\n                    \u2010\u03b2) and impaired mucosal barrier, which exacerbated pathogen colonisation. Together, our findings demonstrate that TAU and GSH alleviate\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>A. hydrophila<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010induced oxidative stress by reducing mitochondrial ROS overproduction and disrupting the ROS\/NF\u2010\u03baB signalling pathway, thereby attenuating inflammatory cytokine storms and ferroptosis. These results provide novel insights into the pathological mechanisms of bacterial sepsis in fish and develop sustainable strategies to improve disease resistance in aquaculture.\n                  <\/jats:p>","DOI":"10.1111\/jfd.70070","type":"journal-article","created":{"date-parts":[[2025,11,4]],"date-time":"2025-11-04T09:51:34Z","timestamp":1762249894000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Taurine and Glutathione Alleviate\n                    <scp>\n                      <i>Aeromonas hydrophila<\/i>\n                    <\/scp>\n                    Infection by Inhibiting Inflammation and Ferroptosis via\n                    <scp>ROS<\/scp>\n                    \/\n                    <scp>NF<\/scp>\n                    \u2010\n                    <scp>\u03baB<\/scp>\n                    Pathway in Fishes"],"prefix":"10.1111","volume":"49","author":[{"given":"Bo","family":"Li","sequence":"first","affiliation":[{"name":"National Aquatic Animal Diseases Para\u2010Reference Laboratory, National Reference Laboratory of Veterinary Drug Residues and MAO Key Laboratory for Detection of Veterinary Drug Residues, Department of Aquatic Animal Medicine, College of Fisheries Huazhong Agricultural University  Wuhan China"},{"name":"College of Animal Science and Technology Yunnan Agricultural University  Kunming China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Penghui","family":"Yu","sequence":"additional","affiliation":[{"name":"National Aquatic Animal Diseases Para\u2010Reference Laboratory, National Reference Laboratory of Veterinary Drug Residues and MAO Key Laboratory for Detection of Veterinary Drug Residues, Department of Aquatic Animal Medicine, College of Fisheries Huazhong Agricultural University  Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Su","sequence":"additional","affiliation":[{"name":"National Aquatic Animal Diseases Para\u2010Reference Laboratory, National Reference Laboratory of Veterinary Drug Residues and MAO Key Laboratory for Detection of Veterinary Drug Residues, Department of Aquatic Animal Medicine, College of Fisheries Huazhong Agricultural University  Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianguo","family":"Su","sequence":"additional","affiliation":[{"name":"National Aquatic Animal Diseases Para\u2010Reference Laboratory, National Reference Laboratory of Veterinary Drug Residues and MAO Key Laboratory for Detection of Veterinary Drug Residues, Department of Aquatic Animal Medicine, College of Fisheries Huazhong Agricultural University  Wuhan 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