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  3. Ureaplasma urealyticum GrpE protein elicits glycolysis-mediated inflammatory responses through TLR2 in macrophages

Ureaplasma urealyticum GrpE protein elicits glycolysis-mediated inflammatory responses through TLR2 in macrophages

  • Immunobiology. 2025 May;230(3):152902. doi: 10.1016/j.imbio.2025.152902.
Jing Xie 1,  Nan Xie 2,  Chang Liu 2,  Zhemin Huang 1,  Min Du 1,  Hao Hu 1,  Kang Zheng 3,  Jiaofeng Peng 4,  Ranhui Li 5
Affiliations

Affiliations

  • 1 Department of Obstetrics, Affiliated Hengyang Hospital of Hunan Normal University & Hengyang Central Hospital, Hengyang, 421001, Hunan, China.
  • 2 Institute of Pathogenic Biology, Hengyang Medical College, University of South China, Hengyang, China.
  • 3 Institute of Pathogenic Biology, Hengyang Medical College, University of South China, Hengyang, China; Department of Clinical Laboratory, Affiliated Hengyang Hospital of Hunan Normal University and Hengyang Central Hospital, Hengyang 421001, Hunan, China.
  • 4 Department of Clinical Laboratory, Affiliated Hengyang Hospital of Hunan Normal University and Hengyang Central Hospital, Hengyang 421001, Hunan, China. Electronic address: 382278527@qq.com.
  • 5 Institute of Pathogenic Biology, Hengyang Medical College, University of South China, Hengyang, China. Electronic address: liranhui@usc.edu.cn.
PMID: 40273504 DOI: 10.1016/j.imbio.2025.152902
Abstract

The pathogenesis of Ureaplasma urealyticum Infection is linked to the host inflammatory response; however, the specific molecular mechanisms underlying this phenomenon have not been fully elucidated. GrpE is a chaperonin that accelerates ADP release and ATP binding to DnaK, thereby enhancing the chaperone function of the HSP70 system under stress. However, alternative activities such as pro-inflammatory responses remain poorly understood. In this study, we report that the U. urealyticum GrpE exerts as a cytokine-inducing virulence factor toward macrophages. Using gene-knockout mice and specific inhibitors, we found that GrpE-induced pro-inflammatory cytokine expression was mediated by the TLR2/STAT3 pathway. We also found that glycolysis was essential for this pro-inflammatory response. Mechanistically, GrpE treatment stimulated STAT3-dependent accumulation of citric acid and acetyl-CoA, promoting histone acetylation and potent pro-inflammatory responses. Our results indicate that glycolysis plays a role in the inflammatory response induced by GrpE through the TLR2/STAT3 pathway and contributes to the glycolysis-mediated inflammatory response, offering a fresh understanding of the development of U. urealyticum Infection.

Keywords

Glycolysis; GrpE; Inflammatory response; TLR2; Ureaplasma urealyticum.

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