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Malaria pigment hemozoin-induced transcriptional remodeling of mouse hematopoietic stem and progenitor cells, granulocyte-macrophage progenitors, and bone marrow monocytes

GSE224161 Mus musculus (mouse) RNA-seq (gene expression) 14 samples Submitted 2025/01/08 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 14 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
14 samples: 6 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
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
Persistent bone marrow hemozoin accumulation confers a survival advantage against bacterial infection via cell-intrinsic Myd88 signalingCell reports · 2024
Summary (written by the submitters)
Trained immunity is the phenomenon whereby innate immune cells such as monocytes or macrophages, and their progenitors in the bone-marrow, undergo functional reprogramming after exposure to certain microbial and danger signals, altering their responses to future exposures. In this study, we performed a non-lethal Plasmodium yoelii 17XNL (Py) infection in wild-type C57/BL6J mice to investigate the underlying mechanism of Py-induced myelopoiesis and performed transcriptomic analysis on HSPCs, GMPs, and monocytes 6 weeks following exposure.
Read the full summary ↓
Next cecal ligation and puncture (CLP) was used to model sepsis in vivo as a secondary exposure, and the transcriptomes of PBS and Py-exposed monocytes were generated.
Published in
Persistent bone marrow hemozoin accumulation confers a survival advantage against bacterial infection via cell-intrinsic Myd88 signaling
Zhu Y, Gao Q, Zhang J et al. · Cell reports 2024 · PMID 39392758 · doi:10.1016/j.celrep.2024.114850
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 GSE224161_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA929995 and SRA study SRP420310. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
GMP_RNA_PBS ×2 GMP_RNA_Plas ×2 Monocyte_RNA_PBS ×2 Monocyte_RNA_Plas ×2 Monocyte_RNA_PBS_CLP ×2 Monocyte_RNA_Plas_CLP ×2 HSPC_RNA_PBS ×1 HSPC_RNA_Plas ×1

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 14 sample titles; they account for 12 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
Datasets on a similar topic

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.