# The Impact of B3GNT7 on Properties of Intestinal Mucus and the Gut Microbiome

> **NIH NIH F30** · UT SOUTHWESTERN MEDICAL CENTER · 2024 · $40,242

## Abstract

Project Summary
The human intestine is colonized by a diverse array of almost 100 trillion bacteria that are critical for health.
Intestinal mucus is the critical interface between the host and the gut microbiome; it is a barrier between
humans and pathogenic microbes, and it is also an attractant for beneficial microbes, supporting vital
commensal microbes with nutrients and attachment sites. The main components of intestinal mucus are highly
O-glycosylated mucins and other glycoproteins. Inflammatory bowel diseases, such as ulcerative colitis and
Crohn’s, are characterized by gut inflammation that results in dysbiosis of the microbiome and alterations in
intestinal mucus glycan structures. The molecular structure of mucus has functional significance. Fucosylation
is abundant in mammalian intestinal mucus, and it has been shown to regulate commensal microbe
colonization and maintain host-microbe symbiosis. Additionally, fucosylation has been shown to alter the
quality and quantity of intestinal mucus in ulcerative colitis patients. Mucin sulfation has also been implicated in
ulcerative colitis. β1-3-N-acetylglucosaminyltransferase 7 (B3GNT7) is an O-glycosyltransferase present on
the Golgi apparatus membrane that transfers GlcNAc to glycan substrates and participates in polyLacNAc
chain biosynthesis. Importantly, these polyLacNAc chains can go on to be further modified by fucose and/or
sulfate. We previously reported that that IL-22, a cytokine critical for maintaining intestinal epithelial
homeostasis, promotes B3GNT7 expression, increases fucosylated O-glycans, and increases polyLacNAc
chains on a model of the human intestinal epithelium. Furthermore, we found that overexpression of B3GNT7
is sufficient to increase cell surface fucosylation. The research outlined in this proposal that B3GNT7 functions
to maintain healthy intestinal mucus and support beneficial commensal gut microbes. This proposal will 1)
Define the impact of B3GNT7 on the biophysical properties of intestinal mucus in cell lines and mice; and 2)
Determine the effect of B3gnt7 expression on host-microbiome interactions. Regulation of intestinal mucus and
the microbiome is poorly understood, and the experiments outline above will elucidate how changes in
glycosylation regulate the microbiome at the molecular and tissue level. Importantly, it will lay the foundation
for future studies of how glycosylation of intestinal mucus contributes to both human health and disease.

## Key facts

- **NIH application ID:** 10856903
- **Project number:** 5F30DK136209-02
- **Recipient organization:** UT SOUTHWESTERN MEDICAL CENTER
- **Principal Investigator:** Mary Wilton Newton Burns
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $40,242
- **Award type:** 5
- **Project period:** 2023-07-01 → 2025-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10856903

## Citation

> US National Institutes of Health, RePORTER application 10856903, The Impact of B3GNT7 on Properties of Intestinal Mucus and the Gut Microbiome (5F30DK136209-02). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10856903. Licensed CC0.

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