ArgR-dependent bacterial resistance to host lipid droplets in Edwardsiella piscicida
Abstract Lipid droplets (LDs), as innate immune hubs, function in the front line of antimicrobial defense involved in the host-pathogen arms race. Particularly for intracellular bacterial pathogens, the endowed capacity to resist host LDs can effectively facilitate pathogen in vivo colonization and...
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2025-02-01
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| Series: | Communications Biology |
| Online Access: | https://doi.org/10.1038/s42003-025-07777-7 |
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| _version_ | 1850237821999120384 |
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| author | Yue Peng Yihan Liu Junze Wu Yuanxing Zhang Qiyao Wang Shuai Shao |
| author_facet | Yue Peng Yihan Liu Junze Wu Yuanxing Zhang Qiyao Wang Shuai Shao |
| author_sort | Yue Peng |
| collection | DOAJ |
| description | Abstract Lipid droplets (LDs), as innate immune hubs, function in the front line of antimicrobial defense involved in the host-pathogen arms race. Particularly for intracellular bacterial pathogens, the endowed capacity to resist host LDs can effectively facilitate pathogen in vivo colonization and evasion from the host’s innate immune response. Here, to investigate the genetic mechanisms of intracellular bacteria response to host LDs, we utilized transposon insertion sequencing to dissect critical fitness determinants of Edwardsiella piscicida under the treatment of LDs isolated from its native host, turbot. Targeted metabolomics indicated that LD challenge resulted in the accumulation of intracellular arginine. The core arginine metabolism regulatory factor, ArgR, was found to play a pivotal role in combating LDs, emphasizing the importance of orchestrating intracellular arginine levels for bacterial LD adaptation. Specifically, ArgR enhanced the expressions of genes involved in arginine catabolism (speA/B and arcC) and diminished gene transcripts associated with arginine import (artP) and synthesis (argD/E/H). Furthermore, ArgR contributed to the pathogenesis of E. piscicida, promoting the proliferation in host cells and virulence in turbot. Collectively, our results shed light on the underlying mechanism of intracellular pathogens resisting LDs during bacterial infections and highlighting the crucial role of arginine in the host-pathogen interactions. |
| format | Article |
| id | doaj-art-720fed3b52ef43cc9e22bdbaa2d28a8f |
| institution | OA Journals |
| issn | 2399-3642 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Communications Biology |
| spelling | doaj-art-720fed3b52ef43cc9e22bdbaa2d28a8f2025-08-20T02:01:39ZengNature PortfolioCommunications Biology2399-36422025-02-018111210.1038/s42003-025-07777-7ArgR-dependent bacterial resistance to host lipid droplets in Edwardsiella piscicidaYue Peng0Yihan Liu1Junze Wu2Yuanxing Zhang3Qiyao Wang4Shuai Shao5State Key Laboratory of Bioreactor Engineering, East China University of Science and TechnologyState Key Laboratory of Bioreactor Engineering, East China University of Science and TechnologyState Key Laboratory of Bioreactor Engineering, East China University of Science and TechnologySouthern Marine Science and Engineering Guangdong Laboratory (Zhuhai)State Key Laboratory of Bioreactor Engineering, East China University of Science and TechnologyState Key Laboratory of Bioreactor Engineering, East China University of Science and TechnologyAbstract Lipid droplets (LDs), as innate immune hubs, function in the front line of antimicrobial defense involved in the host-pathogen arms race. Particularly for intracellular bacterial pathogens, the endowed capacity to resist host LDs can effectively facilitate pathogen in vivo colonization and evasion from the host’s innate immune response. Here, to investigate the genetic mechanisms of intracellular bacteria response to host LDs, we utilized transposon insertion sequencing to dissect critical fitness determinants of Edwardsiella piscicida under the treatment of LDs isolated from its native host, turbot. Targeted metabolomics indicated that LD challenge resulted in the accumulation of intracellular arginine. The core arginine metabolism regulatory factor, ArgR, was found to play a pivotal role in combating LDs, emphasizing the importance of orchestrating intracellular arginine levels for bacterial LD adaptation. Specifically, ArgR enhanced the expressions of genes involved in arginine catabolism (speA/B and arcC) and diminished gene transcripts associated with arginine import (artP) and synthesis (argD/E/H). Furthermore, ArgR contributed to the pathogenesis of E. piscicida, promoting the proliferation in host cells and virulence in turbot. Collectively, our results shed light on the underlying mechanism of intracellular pathogens resisting LDs during bacterial infections and highlighting the crucial role of arginine in the host-pathogen interactions.https://doi.org/10.1038/s42003-025-07777-7 |
| spellingShingle | Yue Peng Yihan Liu Junze Wu Yuanxing Zhang Qiyao Wang Shuai Shao ArgR-dependent bacterial resistance to host lipid droplets in Edwardsiella piscicida Communications Biology |
| title | ArgR-dependent bacterial resistance to host lipid droplets in Edwardsiella piscicida |
| title_full | ArgR-dependent bacterial resistance to host lipid droplets in Edwardsiella piscicida |
| title_fullStr | ArgR-dependent bacterial resistance to host lipid droplets in Edwardsiella piscicida |
| title_full_unstemmed | ArgR-dependent bacterial resistance to host lipid droplets in Edwardsiella piscicida |
| title_short | ArgR-dependent bacterial resistance to host lipid droplets in Edwardsiella piscicida |
| title_sort | argr dependent bacterial resistance to host lipid droplets in edwardsiella piscicida |
| url | https://doi.org/10.1038/s42003-025-07777-7 |
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