ArticleJournal of advanced research2026
HDAC2 enhances the antimicrobial activity of neutrophils by promoting the formation of neutrophil extracellular traps (NETs) in sepsis.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- From immunological mechanisms to targeted therapies: a bibliometric analysis in the domain of research concerning neutrophil extracellular traps and pulmonary diseases (2006-2025).Frontiers in immunology · 2026Pooled it
- Sequential clearance of neutrophil extracellular traps for precision therapy of sepsis.Science advances · 2026Article
- Epigenetic Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Targets.International journal of molecular sciences · 2026Review
- HDAC1 modulates sepsis-induced immunosuppression by driving the exhaustion of CD8+ T cells.JCI insight · 2026Article
- Mitochondrial dysfunction in sepsis-induced immunoparalysis: from immune-cell metabolic reprogramming to clinical biomarkers.Frontiers in immunology · 2026Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSepsis is characterized as a life-threatening organ dysfunction resulting from a dysregulated host response to infection, representing a critical clinical syndrome. Uncontrolled infection and inflammation are two main characteristics of sepsis. Neutrophil extracellular traps (NETs) is a major mechanism by which neutrophils resist pathogens invasion, but the mechanism of the NETs formation remain completely unclear.
objectivesThis study aims to elucidate the role of Histone Deacetylase 2 (HDAC2) in NETs formation and its impact on antimicrobial and anti-inflammatory activities in sepsis.
methodsWe employed flow cytometry, immunofluorescence and western blotting to assess NETs formation. The effects of HDAC2 on NETs and sepsis outcomes were investigated using an HDAC2 inhibitor and HDAC2 knockout mice in CLP-induced and LPS-induced sepsis models. Histone modifications in neutrophils were also analyzed to explore HDAC2's regulatory mechanism.
resultsHDAC2 was found to be highly expressed in patients and mice with sepsis. While HDAC2 knockout or inhibition reduced inflammation and improved organ function in non-infectious sepsis, it decreased survival in infectious sepsis. In addition, knockout or inhibition of HDAC2 significantly reduced the NETs formation, and impaired the antimicrobial activities against E. coli infection in mice. Mechanistically, HDAC2 indirectly promoted H3R17 citrullination to induce the NETs formation through down-regulating H3K18 acetylation and interactively inhibiting CARM1-mediated H3R17 methylation in neutrophils. Furthermore, a dual inhibition strategy targeting HDAC2 and CARM1 not only suppressed inflammation, prevented from multiple organ dysfunction, but also enhanced the antimicrobial activities, which finally improved survival rate of mice with sepsis induced by cecal ligation and puncture (CLP).
conclusionOur findings reveal a novel role for HDAC2 in modulating anti-infectious immunity through NETs formation during sepsis. This study provides a potential therapeutic strategy for sepsis by enhancing both antimicrobial and anti-inflammatory responses, offering a promising approach to preserve organ function and improve survival.
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