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Updated: May 17, 2025

Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages
Published on: October 25, 2017
Autophagy is involved in Salmonella Typhimurium-induced ferroptosis in macrophages
Wei Liu1, Daobin Fu2, Chuanyuan Di2
1College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu Province 225009, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonosis, Yangzhou University, Yangzhou, Jiangsu Province 225009, China.
Abstract:
Salmonella is one of the most common zoonotic pathogens, posing a significant threat to both animal and human health. Our previous study demonstrated that autophagy plays a crucial role in restricting the intracellular growth of Salmonella. This study aims to investigate the effect of autophagy in Salmonella Typhimurium (S. Typhimurium)-induced ferroptosis. First, we found that S. Typhimurium induced lipid peroxidation by increasing intracellular Fe2 + levels, promoting lipid oxidation, and inhibiting the antioxidant pathway. S. Typhimurium-induced lipid peroxidation led to ferroptosis in macrophages. Further results revealed that S. Typhimurium triggered ferritin degradation by NCOA4-mediated ferritinophagy. Additionally, S. Typhimurium-induced chaperone-mediated autophagy (CMA) degraded GPX4 through TAK1-HSC70 signaling pathway. Notably, GPX4 is involved in intracellular S. Typhimurium release. Overall, autophagy was essential for S. Typhimurium induced-ferroptosis, TAK1 not only facilitated autophagy to eliminate intracellular bacteria but also promoted bacterial release.
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