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Loss of pulmonary tissue protection promotes severe Aspergillus fumigatus infection during Influenza A Virus

GSE276049 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/07/16 Platform GPL21103
At a glance

RNA-seq (gene expression) · mouse · 12 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
12 samples: 3 × WT_Mock vs 3 × PR8 vs 3 × AF vs 3 × AF.PR8Groups 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.
Summary (written by the submitters)
Invasive pulmonary aspergillosis (IPA) is a severe fungal disease caused by Aspergillus spp. (particularly A. fumigatus or Af) that may spread hematogenously to extrapulmonary organs. IPA is typically associated with a broad spectrum of immunocompromised conditions and immunologic disorders and constitutes a high mortality rate. While the association of influenza as a risk for secondary bacterial infections is well appreciated, emerging evidence indicates that influenza-hospitalized patients demonstrate increased susceptibility to severe aspergillosis infection.
Read the full summary ↓
In this study, we developed a murine Influenza A Virus (IAV)-Af co-infection model and investigated the role of IAV host response in promoting severe Af infection. Our data show that in a co-infection setting, while IAV suppresses Af-induced CXCL1 and early neutrophil recruitment, no defects in neutrophil phagocytic responses were observed. On the contrary, despite similar fungal burdens and conidial germination between single Af and co-infected lungs, there was greater fungal invasiveness in the early phase of IAV-Af co-infection. These findings suggest that enhanced lung inflammation, vascular injury, and loss of tissue protection in IAV-infecetd lung likely contribute to severe secondary Af infection.
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 GSE276049_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 PRJNA1154583 and SRA study SRP529618. Searching any of these in the dataset finder brings you back here.

Study design
3 × WT_Mock vs 3 × PR8 vs 3 × AF vs 3 × AF.PR8

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 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
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