ENO1 functional plasticity linking metabolism with gene regulation and immunity at the host–pathogen interface
4 affiliations
- 1Key Laboratory of Animal Pathogen Infection and Immunology of Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University
- 2Joint Laboratory of Animal Pathogen Prevention and Control of Fujian-Nepal, College of Animal Sciences, Fujian Agriculture and Forestry University
- 3Key Laboratory of Fujian-Taiwan Animal Pathogen Biology, College of Animal Sciences, Fujian Agriculture and Forestry University
- 4Animal Quarantine Laboratory, Technology Center of Qingdao Customs
Abstract
Enolase 1 (ENO1) is a highly conserved glycolytic enzyme that exhibits remarkable functional plasticity beyond its canonical metabolic role. Increasing evidence indicates that ENO1 participates in diverse cellular and host–pathogen processes, including metabolic adaptation, gene regulation, signaling, immune responses, and pathogen infection. Its functional output is not determined solely by its abundance but is shaped by cellular conditions and functional state, which are influenced by post-translational modifications, subcellular localization, molecular interactions, metabolic conditions, and extracellular or pathogen-derived stimuli. In this review, we summarize current evidence for the context-dependent functions of host ENO1 during infection, with particular emphasis on its roles in metabolic reprogramming, regulation of gene expression and pathogen replication, and modulation of host immunity and inflammation. We further discuss how pathogens can manipulate host ENO1 expression, stability, localization, or molecular interactions to facilitate infection, and distinguish these functions from those of pathogen-derived enolases, which contribute to microbial metabolism, invasion, and host interaction. By integrating these findings, we propose that ENO1 functions as a multifunctional regulatory hub, with its biological activities emerging from the specific molecular and cellular environments in which it operates. This framework provides a mechanistic perspective for understanding how a single conserved protein can engage distinct molecular partners and biological processes across different cellular and infectious settings, highlighting the functional versatility of ENO1 at the host–pathogen interface.
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BibTeX
@article{zhao2026eno1,
title = {{ENO1 functional plasticity linking metabolism with gene regulation and immunity at the host–pathogen interface}},
author = {Conghui Zhao and Peilin Li and Wenjun Shi and Shujie Ma},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1979935},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1979935/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - ENO1 functional plasticity linking metabolism with gene regulation and immunity at the host–pathogen interface
AU - Conghui Zhao
AU - Peilin Li
AU - Wenjun Shi
AU - Shujie Ma
PY - 2026
DA - 2026/10/28
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1979935
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1979935/full
AB - Enolase 1 (ENO1) is a highly conserved glycolytic enzyme that exhibits remarkable functional plasticity beyond its canonical metabolic role. Increasing evidence indicates that ENO1 participates in diverse cellular and host–pathogen processes, including metabolic adaptation, gene regulation, signaling, immune responses, and pathogen infection. Its functional output is not determined solely by its abundance but is shaped by cellular conditions and functional state, which are influenced by post-translational modifications, subcellular localization, molecular interactions, metabolic conditions, and extracellular or pathogen-derived stimuli. In this review, we summarize current evidence for the context-dependent functions of host ENO1 during infection, with particular emphasis on its roles in metabolic reprogramming, regulation of gene expression and pathogen replication, and modulation of host immunity and inflammation. We further discuss how pathogens can manipulate host ENO1 expression, stability, localization, or molecular interactions to facilitate infection, and distinguish these functions from those of pathogen-derived enolases, which contribute to microbial metabolism, invasion, and host interaction. By integrating these findings, we propose that ENO1 functions as a multifunctional regulatory hub, with its biological activities emerging from the specific molecular and cellular environments in which it operates. This framework provides a mechanistic perspective for understanding how a single conserved protein can engage distinct molecular partners and biological processes across different cellular and infectious settings, highlighting the functional versatility of ENO1 at the host–pathogen interface.
SN - 1664-3224
ER -