How DNA repair problems may drive mitochondrial damage and stomach inflammation from H. pylori
Official title: Linking defects in DNA polymerase beta to mitochondrial dysfunction and cytosolic nucleic acid sensor in Helicobacter pylori associated inflammation
Funded at Howard University · NIH-11222671 · Data updated 2026-11-12
This work looks at whether a faulty DNA repair protein lets H. pylori harm cell energy centers and triggers stomach inflammation.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Howard University NIH-funded |
| Lab location | 1 site (Washington, United States) |
| Project start | December 8, 2023 |
| Project end | October 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $428,877 |
| NIH project number | 5R01AI179899-03 |
| Project ID | NIH-11222671 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with current or chronic H. pylori infection or ongoing stomach inflammation would be the most relevant group for future clinical follow-up.
✕Less likely to help
People without H. pylori infection or whose stomach symptoms come from unrelated causes are unlikely to benefit directly from this lab-focused work.
What this research studies
If you have a Helicobacter pylori infection, researchers want to understand how a broken DNA repair step in cells leads to damage in mitochondria and a stronger inflammatory response. They use genetic models of the POLB enzyme (including a 5’-dRP lyase–deficient L22P version), cell systems, and infection experiments with H. pylori to measure mitochondrial DNA damage and immune signaling. The team will track how damaged mitochondrial DNA gets into the cell fluid and activates nucleic acid sensors that drive inflammation. Results will point to molecular steps that could be targeted to reduce infection-related stomach inflammation.
Why it matters
Potential benefit: If successful, this could identify new molecular targets to lessen H. pylori–related stomach inflammation and its complications.
How similar studies have gone: Previous research has linked DNA repair defects to mitochondrial damage and inflammation, but applying the POLB 5’-dRP lyase defect specifically to H. pylori–driven inflammation is a newer, less-tested direction.
Where this research is happening
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Howard University
Washington, United States Active
Researchers
- Principal investigator: Kidane Mulat, Dawit — Howard University
- Study coordinator: Kidane Mulat, Dawit
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.