A STAT2 change that raises risk of bacterial pneumonia after a viral lung infection
The vital role of T403 phosphorylation of STAT2 in post-viral bacterial pneumonia
Researchers are working to understand how a specific change in the immune protein STAT2 may make people more likely to get dangerous bacterial pneumonia after a viral lung infection.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Cleveland Clinic Lerner Com-Cwru NIH-funded |
| Lab location | 1 site (Cleveland, United States) |
| Project ID | NIH-11304498 on NIH RePORTER |
What this research studies
As someone at risk for post-viral bacterial pneumonia, this project looks at how a tiny chemical change (called T403 phosphorylation) on an immune protein named STAT2 after a viral infection might make my body worse at fighting bacteria. The team will study macrophages and neutrophils using lab-grown cells, animal infection models, and analysis of patient-derived samples to see how this change alters antibacterial defenses during flu followed by bacterial infection. They will test whether blocking or reversing the T403 change can restore antibacterial responses in those immune cells. The goal is to identify targets that could lead to ways to prevent or treat dangerous bacterial pneumonia that follows viral illnesses.
Who could benefit from this research
Good fit: Adults who recently had a viral respiratory infection (for example influenza) and then developed bacterial pneumonia, or patients with ARDS willing to provide clinical samples, are the most relevant candidates.
Not a fit: People without recent respiratory infections, young children, or those unable to provide samples or travel to the study site are unlikely to receive direct benefit from this research.
Why it matters
Potential benefit: If successful, this work could point to new ways to prevent or treat bacterial pneumonia that occurs after viral respiratory infections.
How similar studies have performed: Prior studies have linked interferon signaling and STAT proteins to infection outcomes, but the specific T403 phosphorylation is a newly described mechanism that has not yet been tested in patients.
Where this research is happening
Cleveland, United States
- Cleveland Clinic Lerner Com-Cwru — Cleveland, United States (Active)
Researchers
- Principal investigator: Wang, Yuxin — Cleveland Clinic Lerner Com-Cwru
- Study coordinator: Wang, Yuxin
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.