# Contribution of Helicobacter pylori HomA and HomB to colonization and disease

> **NIH NIH R21** · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · 2022 · $190,621

## Abstract

Abstract:
Helicobacter pylori chronically infects 50% of the world’s population and is a significant cause of gastric
cancer. In the stomach, the bacterium interacts with host cells and elaborates virulence factors that directly
influence disease etiology. To maintain colonization within this niche, H. pylori needs mechanisms to
withstand mechanical clearance during the sloughing of epithelial cells and mucous, as well as
mechanisms to prevent detection and clearance by the immune system. Genes encoding for outer
membrane proteins (OMPs) constitute approximately 4% of the H. pylori genome, and it is likely that this
extensive array of proteins may play a crucial role in establishing and maintaining infection by aiding in
adhesion and/or immune evasion. Thus, the OMPs likely serve as key elements of the host-bacterium
interface. In addition, several variable OMPs have been shown to be associated with more severe disease
presentations such as gastric ulcers and gastric cancer. Included among these virulence-associated OMPs
is Helicobacter Outer Membrane Protein B (HomB). HomB is highly similar to HomA and the two have been
shown to have the ability to occupy two primary loci, locus A and locus B in the H. pylori genome; some
strains carry both genes, while some carry one or the other. There are no studies that address the
implications of the two possible genomic locations for homA and homB. Furthermore, despite the fact that
in vitro studies indicate a role for HomB in adherence, virtually no other molecular studies have been
conducted to assess the role of HomA and HomB during H. pylori infection. To gain a better understanding
of the expression and function of these two OMPs, we propose detailed molecular studies that will directly
examine expression of homA and homB in response to environmental stresses that mimic those found
within the gastric environment. Furthermore, using a series of constructed isogenic mutant and
complementation strains that carry all possible single gene combinations of homA and homB, we will
directly assess the role of HomA and HomB in colonization and disease progression in the Mongolian gerbil
model of infection. The described studies will provide novel information concerning expression and function
of HomA and HomB. This information may in turn provide clues to the development of novel therapeutics
that are designed to specifically target these OMPs.

## Key facts

- **NIH application ID:** 10434145
- **Project number:** 5R21AI156357-02
- **Recipient organization:** HENRY M. JACKSON FDN FOR THE ADV MIL/MED
- **Principal Investigator:** ANGELA MELTON-CELSA
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $190,621
- **Award type:** 5
- **Project period:** 2021-06-21 → 2025-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10434145

## Citation

> US National Institutes of Health, RePORTER application 10434145, Contribution of Helicobacter pylori HomA and HomB to colonization and disease (5R21AI156357-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10434145. Licensed CC0.

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