GEO series

Conserved transcriptional response to adversity-related inflammation contributes to Meniere’s disease progression [RNA-Seq 1]

GSE244978 Homo sapiens (human) RNA-seq (gene expression) 10 samples Submitted 2026/02/25 Platform GPL28038

At a glance

RNA-seq (gene expression) · human · 10 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: 10 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: A Stress-Neuroendocrine-Myeloid Inflammation Axis Is Associated with the Progression of Ménière's DiseaseBrain, behavior, & immunity - health · 2026

Summary (written by the submitters)

Meniere’s disease (MD) is a common chronic inner ear disease of largely unknown etiology. Several psychobehavioral stressors and alterations in the immune system have been linked to MD attacks and disease progression. Nevertheless, the molecular basis of alterations in systemic immunity in individuals with MD remains unclear.

Read the full summary ↓

This study aimed to demonstrate the roles of the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis in patients with MD in regulating the lineage commitment and response pattern of myeloid cells and the potential implications on the function of the inner ear in MD. The peripheral blood transcriptome from patients with MD showed elevated levels of inflammation and decreased antiviral response, and myeloid cells were the main source of conserved transcriptional response to adversity (CTRA)-related inflammation. The expression of transcription factors regulating myeloid lineage commitment was altered, and flow cytometry analysis showed an expanded monocyte population, characterized by an increased subset of immature proinflammatory monocytes. Sympathetic signaling was activated in patients with MD, as evident by elevated norepinephrine levels and up-regulated adrenergic receptor β1 expression. LPS-induced inflammation in vitro was almost completely reversed by β blockers and an adenylate cyclase inhibitor in MD myeloid cells, and partially reversed by β1 and β2 subtypes, suggesting that the β-ADR-cAMP signaling pathway mediates exaggerated proinflammatory responses in myeloid cells. Although no significant change was observed in plasma cortisol levels in patients with MD, the increased ratio of the glucocorticoid receptor NR3C1 to the mineralocorticoid receptor NR3C2 suggested that MD myeloid cells were more sensitive to glucocorticoids. In vitro experiments confirmed that glucocorticoids significantly reduce LPS-induced inflammation. G-CSF levels were significantly elevated in patients with MD and correlated well with the levels of other cytokines. Cross-sectional and longitudinal follow-up data showed that the group with high or increased G-CSF over time had worse inner ear function, reflecting the potential effect of systemic inflammation on inner ear function in patients with MD. Our data provide an additional mechanism to elucidate the regulation of the transcriptome of MD myeloid cells by the HPA axis and SNS, and their potential effects on inner ear function. Conclusively, our results imply that good management of stress and prevention of CTRA development may benefit patients with MD.

Published in

A Stress-Neuroendocrine-Myeloid Inflammation Axis Is Associated with the Progression of Ménière's Disease

Li X, Zhang N, Song Y et al. · Brain, behavior, & immunity - health 2026 · PMID 41704658 · doi:10.1016/j.bbih.2026.101193

This dataset

Open GSE244978 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 GSE244978_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 PRJNA1026557 and SRA study SRP465452. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41704658) ↗

Samples in this study

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+ 10 more — browse all 10 samples with per-sample file links →

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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.