# scRNA-seq and scATAC-seq analyses highlight the role of TNF signaling pathway in chronic obstructive pulmonary disease model mice

## TL;DR

This study uses advanced sequencing techniques to show that the TNF signaling pathway is active in a mouse model of COPD, suggesting a potential role in the disease's progression.

## Contribution

The study identifies TNF signaling as a potential contributor to COPD using combined scRNA-seq and scATAC-seq data from a mouse model.

## Key findings

- TNF signaling pathway enrichment was observed in COPD model mice using scRNA-seq and scATAC-seq.
- TNFR1 upregulation and increased Il1b, Csf1, and Bcl3 site accessibility were found in relevant cell types.
- Monocytes/macrophages, dendritic cells, and B cells showed similar trends in TNF signaling pathway activity.

## Abstract

Chronic obstructive pulmonary disease (COPD) is a prevalent and progressive form of respiratory disease in which patients exhibit persistent respiratory damage affecting the alveoli and/or airway due to exposure to toxic gases or particulate matter. C57BL/6 mice were exposed to cigarette smoke and lipopolysaccharide to establish a COPD model mice, followed by scATAC (Assay for Transposase Accessible Chromatin) sequencing and scRNA sequencing of lung tissue samples. The resultant data revealed consistent findings between scATAC-seq and scRNA-seq regarding cell types, differentially expressed genes, and signaling pathways in COPD model mice. Tumor necrosis factor (TNF) signaling pathway enrichment was evident in the scRNA-seq and scATAC-seq datasets, with similar trends in monocytes/macrophages, dendritic cells, and B cells. In COPD model mice, significant tumor necrosis factor receptor 1 (TNFR1) upregulation and high levels of activity related to cellular communication were observed, and significant increases in Il1b, Csf1, and Bcl3 site accessibility were evident in cells. These findings suggest that the TNF signaling pathway maybe associated with COPD.