# Investigating the role of lipooligosaccharide sialylation in Neisseria gonorrhoeae-neutrophil interactions

> **NIH NIH F31** · UNIVERSITY OF VIRGINIA · 2021 · $34,673

## Abstract

Abstract
Gonorrhea, caused by the bacterium Neisseria gonorrhoeae (Gc), is characterized by the influx of neutrophils
to sites of infection. Gc has many nonredundant mechanisms to manipulate neutrophil activation and resist
killing by neutrophil antimicrobial components. In neutrophil-rich male urethral exudates, the oligosaccharide of
Gc lipooligosaccharide (LOS) becomes modified by sialic acid in a process known as sialylation. Gc
incorporates host derived sialic acid into LOS using the surface-exposed enzyme LOS sialyltransferase (Lst).
While sialylation by Lst has been shown to protect Gc from complement-mediated killing and enhances Gc
infectivity in in vitro and animal models of infection, how it affects the ability of Gc to survive in association with
neutrophils is unclear. My preliminary results show that sialylated Gc significantly reduces the oxidative burst of
primary human neutrophils, suggesting modulation of neutrophil anti-gonococcal properties. In this proposal, I
will test the hypothesis that LOS sialylation protects Gc from killing by primary human neutrophils, with
potential mechanisms including increased resistance to neutrophil antimicrobial components and limiting the
production and/or release of these components by neutrophils. I will simultaneously test the hypothesis that
neutrophils modify the sialylation state of Gc by providing sialic acid as substrate and through their
sialyltransferase and sialidase activities. To address these hypotheses, I have created isogenic Gc strains that
produce single, physiologically relevant OS chemotypes and express or are deficient for Lst. My collaborators
and I have also developed a method to monitor the sialylation state of Gc during infection using click chemistry,
the first time sialylation on Gc can be directly monitored in real-time. Results from this project will show how
modification by sialylation drives the ability of Gc to evade killing by neutrophils and persist in its obligate
human host, and will provide me with the scientific and professional training for my PhD to ultimately be a
leader in the host-pathogen interactions field.

## Key facts

- **NIH application ID:** 10312906
- **Project number:** 1F31AI157528-01A1
- **Recipient organization:** UNIVERSITY OF VIRGINIA
- **Principal Investigator:** Amaris J. Cardenas
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $34,673
- **Award type:** 1
- **Project period:** 2021-11-01 → 2023-10-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10312906

## Citation

> US National Institutes of Health, RePORTER application 10312906, Investigating the role of lipooligosaccharide sialylation in Neisseria gonorrhoeae-neutrophil interactions (1F31AI157528-01A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10312906. Licensed CC0.

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