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Adipose tissue inflammation mediated by CCL19 overexpression exacerbates experimental periodontitis via elevated circulating saturated fatty acids and osteopontin in Western-diet-fed mice

GSE328134 Mus musculus (mouse) RNA-seq (gene expression) 36 samples Submitted 2026/04/22 Platform GPL34871
At a glance

RNA-seq (gene expression) · mouse · 36 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
36 samples: 12 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
Adipose tissue inflammation mediated by CCL19 overexpression exacerbates experimental periodontitis via elevated circulating saturated fatty acids and osteopontin in Western-diet-fed miceFrontiers in immunology · 2026
Summary (written by the submitters)
Introduction: Individuals with obesity may be at a higher risk of developing severe periodontitis. We previously reported that C-C motif ligand 19 (CCL19) plays a pivotal role in adipose inflammation in obesity and that adipocyte-specific Ccl19 knock-in (CCL19-KI) mice exhibited greater inflammatory cell infiltration in visceral fat, increased weight gain, and abnormal glucose metabolism than wild-type (WT) mice under a 40% high-fat diet (HFD).
Read the full summary ↓
In this study, we examined the susceptibility of mice fed diets with different fat contents to the severity of experimental periodontitis. Methods: Six-week-old male WT and CCL19-KI mice were fed either a normal diet (ND), 40% HFD, or 60% HFD for 8 weeks, after which ligature-induced periodontitis (LIP) was established. Two weeks after ligation, alveolar bone resorption, gingival inflammatory and osteoclastogenic gene expression, and serum free fatty acid (FFA) levels were compared among the groups. Additionally, RNA-sequencing (RNA-seq) was performed on epididymal white adipose tissue (eWAT) of each ligatured mouse to explore potential factors mediating periodontitis aggravation. Furthermore, in vitro studies using macrophages were conducted to investigate a possible mechanism in the progression of periodontitis. Results: Alveolar bone resorption, gingival inflammatory and osteoclastogenic gene expression, and serum FFA levels were significantly higher in ligated CCL19-KI mice than those in ligated WT mice under a 40% HFD. RNA-seq revealed that the OPN gene (Spp1) expression in eWAT was significantly upregulated in CCL19-KI mice fed an ND or 40% HFD compared with that in WT mice, which was consistent with serum OPN levels. Peritoneal macrophages from 40% HFD-fed CCL19-KI mice secreted significantly higher amounts of TNF-a than those from WT mice fed the same diet under Escherichia coli lipopolysaccharide (LPS) stimulation. Both palmitic acid priming and OPN significantly promoted osteoclastogenesis in RANKL-treated BMMs, and their combination further enhanced this effect. Conclusions: CCL19-modified adipose tissue inflammation may contribute to the severity of periodontitis via the upregulation of circulating saturated fatty acids and Spp1, resulting in enhanced TNF-a production in macrophages and increased osteoclastogenesis in BMMs under mild to moderate obesity.
Published in
Adipose tissue inflammation mediated by CCL19 overexpression exacerbates experimental periodontitis via elevated circulating saturated fatty acids and osteopontin in Western-diet-fed mice
Ryo N, Shinjo T, Shida M et al. · Frontiers in immunology 2026 · PMID 42148137 · doi:10.3389/fimmu.2026.1787572
This dataset
Open GSE328134 in finder → Find more mouse 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 GSE328134_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 PRJNA1453980 and SRA study SRP692112. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42148137) ↗
Study design
12 conditions, mostly in triplicate
NW ×3 NWL ×3 NK ×3 NKL ×3 s40W ×3 s40WL ×3 s40K ×3 s40KL ×3 +4 more

Supports a between-group comparison across 36 samples.

How we read this: 12 replicated groups read from 36 sample titles; they account for 36 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
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