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

Award Number: F31AI176804
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 07/29/2024
PERIOD OF PERFORMANCE END DATE: 07/28/2026

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How ribosomal silencing promotes chronic infection of the gastric pathogen Helicobacter pylori - 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-growth states, test the field’s current model that proposes low growth states are used in chronic infection, and define the role of an essential physiological mechanism required by H. pylori to maintain disease-causing infections.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = $42,795 )
2025	2025	UNIVERSITY OF CALIFORNIA SANTA CRUZ	1156 HIGH ST	SANTA CRUZ	CA	95064	SANTA CRUZ	USA	Allergy and Infectious Diseases Research	002	2	8/25/2025	NON-COMPETING CONTINUATION	$42,795
2025	2024	UNIVERSITY OF CALIFORNIA SANTA CRUZ	1156 HIGH ST	SANTA CRUZ	CA	95064	SANTA CRUZ	USA	Allergy and Infectious Diseases Research	001	1	7/9/2025	OTHER REVISION	$0
2025	2024	UNIVERSITY OF CALIFORNIA SANTA CRUZ	1156 HIGH ST	SANTA CRUZ	CA	95064	SANTA CRUZ	USA	Allergy and Infectious Diseases Research	000	1	4/18/2025	TERMINATION	$0
														Subtotal = $42,795

Issue Date FY: 2024 ( Subtotal = $41,873 )
2024	2024	UNIVERSITY OF CALIFORNIA SANTA CRUZ	1156 HIGH ST	SANTA CRUZ	CA	95064	SANTA CRUZ	USA	Allergy and Infectious Diseases Research	001	1	7/29/2024	NEW	$0
2024	2024	UNIVERSITY OF CALIFORNIA SANTA CRUZ	1156 HIGH ST	SANTA CRUZ	CA	95064	SANTA CRUZ	USA	Allergy and Infectious Diseases Research	000	1	7/29/2024	NEW	$41,873
														Subtotal = $41,873

Grand Total All Awards = $84,668

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

Award Number: F31AI176804

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 07/29/2024

PERIOD OF PERFORMANCE END DATE: 07/28/2026

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