A molecular switch in lung blood-vessel cells that drives dangerous inflammation
S1PR1 Mislocalization in Lung Endothelium Regulates Innate Immune Function and Mediates Inflammatory Lung Injury
This work looks at whether a change in a receptor on lung blood-vessel cells causes those cells to trigger harmful inflammation during severe lung infections or acute lung injury, potentially affecting people with ARDS or severe pneumonia.
Quick facts
| Grant type | P01 program project |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Illinois at Chicago NIH-funded |
| Lab location | 1 site (Chicago, UNITED STATES) |
| Project ID | NIH-11167447 on NIH RePORTER |
What this research studies
If I had a severe lung infection or injury, this project would trace how a receptor called S1PR1 on lung blood-vessel (endothelial) cells is chemically changed after inflammation. The team follows steps including phosphorylation of S1PR1, its movement into the cell's endoplasmic reticulum, binding to the chaperone BiP, and downstream signaling through G-proteins and calcium. They use lab cell experiments, advanced microscopy, and animal models to map this chain of events and test whether interrupting these steps prevents lasting lung damage. The goal is to link these molecular events to inflammatory lung injury from bacteria and cytokines so future therapies could target the switch.
Who could benefit from this research
Good fit: People hospitalized with acute lung injury, acute respiratory distress syndrome (ARDS), or severe pneumonia would be the most relevant candidates for related clinical studies or for donating samples.
Not a fit: People without inflammatory lung conditions, or whose lung problems are chronic and unrelated to acute infection-driven inflammation, are unlikely to benefit directly from this work.
Why it matters
Potential benefit: If successful, this work could point to new treatments that stop runaway lung inflammation and reduce deaths or long-term damage from acute lung injury and ARDS.
How similar studies have performed: Previous research showed S1PR1 can protect the vascular barrier, but the idea that its mislocalization drives harmful inflammation is a novel finding that has not yet been tested in patients.
Where this research is happening
Chicago, UNITED STATES
- University of Illinois at Chicago — Chicago, United States (Active)
Researchers
- Principal investigator: Mehta, Dolly — University of Illinois at Chicago
- Study coordinator: Mehta, Dolly
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.