# How ribosomal silencing promotes chronic infection of the gastric pathogen Helicobacter pylori

> **NIH NIH F31** · UNIVERSITY OF CALIFORNIA SANTA CRUZ · 2024 · $41,873

## Abstract

Project Summary: Helicobacter pylori is a bacterial pathogen that infects nearly 50% of the global population
and establishes disease-causing infections in the gastric epithelium. H. pylori infections are cured using so-
called triple antibiotic therapies, but these fail to eradicate H. pylori in approximately 20-25% of treated
patients. Chronic H. pylori infections cause severe gastrointestinal illnesses, gastric adenocarcinomas, and
gastric mucosal lymphomas. Despite the devastating consequences of uneradicated H. pylori infections, the
mechanisms that allow H. pylori to persist are not well characterized despite the pathogen’s contribution to the
disease. Due to increasing in vivo evidence from clinical trials and gastric mucosal biopsies, the field presently
proposes that low-growth states such as biofilms facilitate chronic infections in the host. H. pylori biofilm growth
is not fully characterized, but our lab showed that genes for ribosomal proteins and ribosome regulators are
differentially expressed between biofilm and non-biofilm growth. A gap in knowledge in this field is how H.
pylori regulates its ribosome population in low-growth states such as biofilms, and what advantage this
regulation confers particularly to maintain chronic infections. My proposed research will address this
mechanistic knowledge gap and provide necessary fundamental understanding into how ribosomes are
regulated under growth-limiting conditions and in the host. The long-term objective of this study is to
determine how H. pylori utilizes ribosomal silencing to regulate ribosome assembly, survive stresses in the
host and maintain chronic infections. Preliminary studies show that rsfS, the only known ribosome silencing
factor in H. pylori, is required for growth limiting conditions, biofilm growth, and long-term in vivo colonization.
The hypothesis for this study is that RsfS is utilized in low growth states to regulate the ribosome population
so that H. pylori can maintain chronic infections and survive eradication. The approach will be to expand upon
preliminary findings by determining the temporal expression and control elements of rsfS under growth limiting
conditions and further investigate the role of rsfS expression in vivo. AIM 1 will identify specific growth limiting
conditions in which ribosome silencing is being utilized by defining the conditions that lead to differential rsfS
expression and affect the ribosome population. AIM 2 will further define the role of rsfS expression in long-term
in vivo infections to help identify the stage of infection that H. pylori utilizes ribosome silencing. The rationale
for the proposed aims is that the findings will elucidate mechanisms that allow bacteria in chronic infections
to persist so that more effective therapeutic strategies can be developed. The contributions from the fulfillment
of these aims will be significant because they will provide fundamental insight regarding H. pylori ribosome
populations in low-gr...

## Key facts

- **NIH application ID:** 10998526
- **Project number:** 1F31AI176804-01A1
- **Recipient organization:** UNIVERSITY OF CALIFORNIA SANTA CRUZ
- **Principal Investigator:** Yasmine Elshenawi
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $41,873
- **Award type:** 1
- **Project period:** 2024-07-29 → 2026-07-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10998526

## Citation

> US National Institutes of Health, RePORTER application 10998526, How ribosomal silencing promotes chronic infection of the gastric pathogen Helicobacter pylori (1F31AI176804-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10998526. Licensed CC0.

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