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Contribution of Stroma to Inflammatory Bowel Disease Progression Revealed in Patient-Derived Human Colon Chips

GSE277964 Homo sapiens (human) RNA-seq (gene expression) 66 samples Submitted 2025/01/02 Platform GPL16791
At a glance

RNA-seq (gene expression) · human · 66 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
Homo sapiens (human)
Samples
66 samples: 24 conditions, mostly in triplicateGroups 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
Human Organ Chips Reveal New Inflammatory Bowel Disease DriversmedRxiv : the preprint server for health sciences · 2025
Summary (written by the submitters)
Inflammatory bowel disease (IBD) patients exhibit compromised intestinal barrier function, enhanced inflammation, and increased cancer risk, with symptoms sometimes being exacerbated in women during pregnancy. To investigate the IBD phenotype and disease progression in human intestine, we leveraged organ-on-a-chip (Organ Chip) technology to engineer human Colon Chips lined by homotypic or heterotypic recombinants of intestinal epithelium interfaced with stromal fibroblasts isolated from Healthy or IBD patient-derived colon resections.
Read the full summary ↓
Chips created with both epithelial and stromal cells from the same ulcerative colitis or Crohn's disease patient showed increased IBD-associated gene pathway activation, elevated pro-inflammatory cytokines, reduced mucus layer thickness, increased intestinal barrier permeability, compared to homotypic Healthy Colon Chips. When heterotypic tissue recombinants were created, the IBD stromal fibroblasts induced the IBD phenotype in healthy epithelium, and healthy colonic fibroblasts partially reduced inflammation in the IBD epithelium. Using this system, we discovered that peristalsis-like mechanical deformations directly impact colon tissue physiology by increasing mucin gene expression, mucus thickness, and barrier permeability in both Healthy and IBD Chips, and that they only stimulate a fibrotic response in IBD Chips. We also found that both inflammation and fibrosis were accentuated in IBD Chips created with cells from a female patient that were exposed to pregnancy-associated hormones. Interestingly, exposure to a carcinogen (N-ethyl-N-nitrosourea) for 3 weeks in vitro induced histological changes and gene duplication in the IBD Chips, but not in the Healthy Chips. These data suggest that the stroma plays a key role in driving inflammation and disease progression in IBD patients and that human Organ Chip technology may represent a new preclinical tool to gain insight into these mechanisms as well as to identify novel diagnostic biomarkers and therapeutics.
Published in
Human Organ Chips Reveal New Inflammatory Bowel Disease Drivers
Özkan A, Merry GE, Chou DB et al. · medRxiv : the preprint server for health sciences 2025 · PMID 39677416 · doi:10.1101/2024.12.05.24318563
This dataset
Open GSE277964 in finder → Find more human RNA-seq datasets →
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.

Series matrix ↓
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 GSE277964_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

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 PRJNA1164829 and SRA study SRP534562. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39677416) ↗
Study design
24 conditions, mostly in triplicate
Colon fibroblast, IBD, ulcerative colitis, no… ×3 Colon fibroblast, IBD, ulcerative colitis, st… ×3 Colon epithelium, IBD, ulcerative colitis, no… ×3 Colon fibroblast, IBD, ulcerative colitis, no… ×3 Colon epithelium, healthy, strain, donor H3, ×3 Colon fibroblast, healthy, strain, donor H3, ×3 Colon epithelium, healthy, no strain, donor H… ×3 Colon fibroblast, healthy, no strain, donor H… ×3 +16 more

Supports a between-group comparison across 66 samples.

How we read this: 24 replicated groups read from 66 sample titles; they account for 66 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

+ 26 more — browse all 66 samples with per-sample file links →

Datasets on a similar topic

Search all human RNA-seq datasets in GEO →

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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.