Evidence map›Paper›PMID 39028614›Full record

ArticleClinical and experimental immunology2025

C/EBPε and its acetylation in PMN enhance the tolerance to trauma.

Shaowen Cheng, Junyu Zhu, Yangyang Bian, Jiangling Yao, Wei Zhang, Shuangqin Yin, Tianyin Kuang, Lina Xian, Huaping Liang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Shaowen ChengState Key Laboratory of Trauma, Burns and Combined Injury, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, China.
Junyu ZhuState Key Laboratory of Trauma, Burns and Combined Injury, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, China.
Yangyang BianDepartment of Wound Repair, Key Laboratory of Emergency and Trauma of Ministry of Education, The First Affiliated Hospital of Hainan Medical University, Haikou, China.
Jiangling YaoDepartment of Wound Repair, Key Laboratory of Emergency and Trauma of Ministry of Education, The First Affiliated Hospital of Hainan Medical University, Haikou, China.
Wei ZhangEmergency and Trauma College, Hainan Medical University, Haikou, China.
Shuangqin YinState Key Laboratory of Trauma, Burns and Combined Injury, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, China.
Tianyin KuangState Key Laboratory of Trauma, Burns and Combined Injury, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, China.
Lina XianIntensive Care Unit, The First Affiliated Hospital of Hainan Medical University, Haikou, China.
Huaping LiangState Key Laboratory of Trauma, Burns and Combined Injury, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, China.ORCID 0000-0003-4157-445X

Funding

Hainan Province Clinical Medical CenterHainan Provincial Natural Science Foundation of China 822MS174National Natural Science Foundation of China 82260373
6 · The paper itself

Abstract

Severe trauma can lead to numerous serious complications, threating the well-being and vitality of the afflicted. The quantity and functionality of polymorphonuclear neutrophils (PMNs) undergo rapid transformations in response to severe trauma, playing a pivotal role in the trauma response. The absence of CCAAT/enhancer-binding protein ε (C/EBPε) profoundly impairs the functionality of PMNs, a function of paramount importance in trauma. In this study, by generating mice with C/EBPε knocked out or overexpressed, we substantiate that C/EBPε ensures the restoration of PMN function, enhancing the expression of antimicrobial proteins and thereby promoting trauma recovery. Furthermore, diminished expression of C/EBPε is observed in trauma patients, with levels displaying a negative correlation with ISS and APACHE II scores, suggesting its potential as a prognostic indicator for clinical treatment. Mechanistically, we uncover the upregulation of SIRT1 and the inhibition of P300 participating in the suppression of C/EBPε acetylation, consequently reducing the resilience of mice to trauma. Therapeutic interventions, whether through the sole administration of PMN, nicotinamide (NAM) treatment, or their combination, all result in an increased survival rate in traumatic mice. In conclusion, our study elucidates the role of C/EBPε in enhancing the resilience to trauma and identifies C/EBPε acetylation as a critical regulatory mechanism, offering potential therapeutic approaches involving PMN transfusion and NAM treatment.

Indexed as

CCAAT-Enhancer-Binding ProteinsImmune ToleranceNeutrophilsWounds and InjuriesAcetylationAnimalsFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutSirtuin 1CCAAT-Enhancer-Binding ProteinsSirt1 protein, mouseSirtuin 1acetylationC/EBPεpolymorphonuclear neutrophilstrauma

Identifiers

PMID39028614
PMCPMC11771198

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.