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Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity [ChIP-seq]

GSE240723 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 20 samples Submitted 2025/09/30 Platform GPL20301
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 20 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Homo sapiens (human)
Samples
20 samples
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunityNature immunology · 2025
Summary (written by the submitters)
A deeper understanding of the processes that sustain long-term reprogramming of rapidly turned-over cells in humans can offer unprecedented therapeutic potential, especially for immune cells like neutrophils, given their short lifespan in circulation and importance in both acute and chronic diseases. Hypoxia is a hallmark of a plethora of disease states and significantly shapes neutrophil effector functions.
Read the full summary ↓
However, its potential contribution to long-term neutrophil reprogramming remains largely unexplored. We have observed persistent perturbations in newly formed circulating neutrophils’ phenotype and function in patients 3-6 months following hospitalisation with acute respiratory distress syndrome (ARDS), where poor oxygenation takes place. These lasting changes are associated with widespread loss of H3K4me3 in genomic regions of relevance to neutrophil activities. Notably, the replication of these findings in healthy volunteers months following altitude-induced hypoxaemia attributes a role to the oxygen deprivation as a driver for long-term neutrophil reprogramming. Mechanistically, mouse models of systemic hypoxia reveal deleterious outcomes for infection and show that persistent loss of H3K4me3 originates in proNeu and preNeu populations within the bone marrow and is linked to hypoxia-driven n-terminal histone 3 clipping. Thus, we present novel evidence that acute adaptations to systemic hypoxia trigger central changes in newly formed neutrophil populations, resulting in long-term impairment of effector functions and placing hypoxia as a crucial orchestrator of sustained neutrophil reprogramming.
Published in
Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity
Sanchez-Garcia MA, Sadiku P, Ortmann BM et al. · Nature immunology 2025 · PMID 41152617 · doi:10.1038/s41590-025-02301-9
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE240723_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1004667 and SRA study SRP454702. Searching any of these in the dataset finder brings you back here.

Samples in this study

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