MINI REVIEW article
Front. Immunol.
Sec. Inflammation
Lactylation modification - a bridge between sepsis and macrophage metabolic reprogramming
Zhe Fang 1
Biao Xu 2
Gui song Zhu 2
Dengyun Nie 2
1. Nanjing University of Chinese Medicine, Nanjing, China
2. Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, China
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Abstract
Sepsis is a life-threatening organ failure syndrome triggered by dysregulated host responses to infection. During disease progression, macrophages drive initial hyperinflammatory responses and critically regulate the subsequent immunosuppressive phase. Emerging evidence reveals that macrophage phenotypes dynamically adapt through metabolic reprogramming, creating phenotype-metabolism interdependence. Notably, lactate—long considered merely a glycolytic byproduct—now emerges as a key regulator through histone lactylation. This epigenetic modification fine-tunes macrophage functionality and corrects inflammatory imbalance in sepsis. This breakthrough illuminates lactylation's central role in macrophage regulation, opening new diagnostic and therapeutic avenues. This review comprehensively examines lactylation mechanisms and their impact on metabolic control in sepsis-associated macrophages.
Summary
Keywords
Glycolysis, Lactation modification, Macrophages, metabolic reprogramming, Sepsis
Received
03 November 2025
Accepted
20 February 2026
Copyright
© 2026 Fang, Xu, Zhu and Nie. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Biao Xu
Disclaimer
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