How mucus plugs form in type 2 (allergic) asthma
Project 1: Novel mechanisms driving mucin secretion and mucus plugging in type 2-high asthma
This project looks at how allergic (type 2) asthma causes airway cells to release sticky mucus that can block breathing, aiming to help people with severe asthma.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California, San Francisco NIH-funded |
| Lab location | 1 site (San Francisco, United States) |
| Project ID | NIH-11325849 on NIH RePORTER |
What this research studies
They will study airway cells taken from people with type 2-high asthma and use mouse models to see how a protein called TSPAN8 helps goblet cells release mucin. The team will use CRISPR gene tools to change genes involved in mucus secretion and examine how cathepsin proteases and their human inhibitors (cystatins) alter mucus composition. By combining experiments on human airway cells and animals, they aim to connect specific molecular changes to the formation of mucus plugs. Findings could point to new drug targets to prevent airway blockage in severe asthma.
Who could benefit from this research
Good fit: Ideal candidates would be people with type 2-high or severe asthma, especially those who have evidence of mucus plugging or frequent airway obstruction, who could provide airway samples or be considered for future therapies.
Not a fit: People whose asthma is not driven by type 2 inflammation or whose breathing problems are due to non-mucus causes are less likely to benefit from findings focused on mucus plugging mechanisms.
Why it matters
Potential benefit: If successful, this work could identify targets for treatments that reduce mucus plugging and improve breathing in people with severe type 2 asthma.
How similar studies have performed: Previous research has linked the type 2 cytokine IL-13 to mucus changes and plugging, but targeting TSPAN8 and the cystatin/cathepsin pathways is a newer, less-tested approach.
Where this research is happening
San Francisco, United States
- University of California, San Francisco — San Francisco, United States (Active)
Researchers
- Principal investigator: Erle, David J — University of California, San Francisco
- Study coordinator: Erle, David J
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.