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Peer-reviewedCC BY 4.0Transboundary and Emerging Diseases

Macrophage USF2 Lactylation‐Mediated FABP4 Suppression Promotes Intracellular Proliferation of Brucella

  • Yuanhao Yang1,2
  • Yaping Zu1,2
  • Xin Wang1,2
  • Xiaofang Liu1,2
  • Yunyi Zhai1,2
  • Ye Yuan1,2
  • Gaowa Wudong1,2
  • Wei Liu1,2
  • Yaping Jin1,2
  • Dong Zhou1,2
  • Aihua Wang1,2
  1. 1College of Veterinary Medicine Northwest A&F University Yangling 712100 Shaanxi China nwsuaf.edu.cn
  2. 2Key Laboratory of Animal Biotechnology of the Ministry of Agriculture Northwest A&F University Yangling 712100 Shaanxi China nwsuaf.edu.cn
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Abstract

Brucella spp. are facultative intracellular bacteria that infect and induce brucellosis in a diverse range of mammalian hosts. Understanding the mechanisms underlying the intracellular survival of Brucella is of critical importance for the prevention and control of brucellosis. This study uncovers the mechanism by which Brucella abortus manipulates host lactate metabolism to facilitate its intracellular proliferation. Infection of macrophages by B. abortus enhanced L‐lactate production by the host macrophages, which in turn promoted bacterial proliferation. Proteomic and functional analyses identified the host glucose transporter protein Slc2a1 as a positive regulator of both B. abortus proliferation and host cellular lactylation. The B. abortus effector protein SepA upregulated Slc2a1 expression and host cellular lactylation. Lactylation of the transcription factor USF2 at lysine residues 255 and 275 suppressed production of the host lipid metabolism‐associated protein Fabp4, thereby enhancing bacterial survival. Moreover, Fabp4 inhibition attenuated B. abortus‐induced M1 polarization and lipid metabolism in macrophages. These findings reveal a dual‐axis regulatory network through which B. abortus exploits host L‐lactate metabolic reprogramming via the SepA/Slc2a1 and L‐lactate‐USF2/Fabp4 axes to establish its intracellular niche, providing new insights into host–Brucella metabolic crosstalk.

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Cite

BibTeXRIS
BibTeX
@article{yang2026macrophage,
  title = {{Macrophage USF2 Lactylation‐Mediated FABP4 Suppression Promotes Intracellular Proliferation of Brucella}},
  author = {Yuanhao Yang and Yaping Zu and Xin Wang and Xiaofang Liu and Yunyi Zhai and Ye Yuan and Gaowa Wudong and Wei Liu and Yaping Jin and Dong Zhou and Aihua Wang},
  journal = {Transboundary and Emerging Diseases},
  year = {2026},
  month = nov,
  doi = {10.1155/tbed/3930677},
  url = {https://doi.org/10.1155/tbed/3930677},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Macrophage USF2 Lactylation‐Mediated FABP4 Suppression Promotes Intracellular Proliferation of Brucella
AU  - Yuanhao Yang
AU  - Yaping Zu
AU  - Xin Wang
AU  - Xiaofang Liu
AU  - Yunyi Zhai
AU  - Ye Yuan
AU  - Gaowa Wudong
AU  - Wei Liu
AU  - Yaping Jin
AU  - Dong Zhou
AU  - Aihua Wang
PY  - 2026
DA  - 2026/11/04
JO  - Transboundary and Emerging Diseases
DO  - 10.1155/tbed/3930677
UR  - https://doi.org/10.1155/tbed/3930677
AB  - Brucella spp. are facultative intracellular bacteria that infect and induce brucellosis in a diverse range of mammalian hosts. Understanding the mechanisms underlying the intracellular survival of Brucella is of critical importance for the prevention and control of brucellosis. This study uncovers the mechanism by which Brucella abortus manipulates host lactate metabolism to facilitate its intracellular proliferation. Infection of macrophages by B. abortus enhanced L‐lactate production by the host macrophages, which in turn promoted bacterial proliferation. Proteomic and functional analyses identified the host glucose transporter protein Slc2a1 as a positive regulator of both B. abortus proliferation and host cellular lactylation. The B. abortus effector protein SepA upregulated Slc2a1 expression and host cellular lactylation. Lactylation of the transcription factor USF2 at lysine residues 255 and 275 suppressed production of the host lipid metabolism‐associated protein Fabp4, thereby enhancing bacterial survival. Moreover, Fabp4 inhibition attenuated B. abortus‐induced M1 polarization and lipid metabolism in macrophages. These findings reveal a dual‐axis regulatory network through which B. abortus exploits host L‐lactate metabolic reprogramming via the SepA/Slc2a1 and L‐lactate‐USF2/Fabp4 axes to establish its intracellular niche, providing new insights into host–Brucella metabolic crosstalk.
SN  - 1865-1674
SN  - 1865-1682
ER  -