How H. pylori senses signals to colonize the stomach and cause ulcers and cancer
Official title: The function of chemotactic signal transduction during colonization and disease
Funded at University of California Santa Cruz · NIH-11372644 · Data updated 2026-11-12
This research looks at how the stomach bacterium H. pylori uses a sensor called TlpC to survive immune attack and promote ulcers and stomach cancer, which matters for people with H. pylori infection.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California Santa Cruz NIH-funded |
| Lab location | 1 site (Santa Cruz, United States) |
| Project start | December 1, 2015 |
| Project end | August 31, 2026 |
| Funding year | 2025 |
| Award (this year) | $14,320 |
| NIH project number | 3R01AI116946-10S1 |
| Project ID | NIH-11372644 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with current H. pylori infection—especially those with persistent infection after treatment or with peptic ulcers—would be the eventual population to benefit or to be eligible for future related clinical studies, though this grant itself is laboratory-focused.
✕Less likely to help
People without H. pylori infection or whose stomach problems are caused by non-bacterial factors are unlikely to gain direct benefit from this project.
What this research studies
Scientists will study a bacterial sensor protein named TlpC that helps H. pylori detect lactate and other signals from the stomach environment. In lab experiments they will determine how TlpC binds signals, test mutant bacteria that alter TlpC function, and measure how these changes affect survival against the immune system component called complement. The team will also use in vivo models and bacterial samples to see where and when TlpC-driven sensing helps bacterial growth during infection. The goal is to connect molecular details to how H. pylori colonizes the human stomach and leads to ulcers or gastric cancer.
Why it matters
Potential benefit: If successful, this work could reveal new targets to block H. pylori survival in the stomach and lead to therapies that reduce ulcers and stomach cancer.
How similar studies have gone: Previous research has shown H. pylori chemoreceptors influence colonization, but the idea that TlpC's lactate sensing promotes complement resistance is a relatively new finding with limited clinical testing to date.
Where this research is happening
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University of California Santa Cruz
Santa Cruz, United States Active
Researchers
- Principal investigator: Ottemann, Karen M — University of California Santa Cruz
- Study coordinator: Ottemann, Karen M
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.