# Host-associated biofilm formation and dispersal mechanisms

> **NIH NIH R35** · LOYOLA UNIVERSITY CHICAGO · 2024 · $432,426

## Abstract

Abstract
Pathogenic and symbiotic bacteria interact with animal hosts and protect themselves from external and host
environments—other microbes, host-defense cells, toxic molecules, and importantly, therapeutic antibiotics—by
adhering to each other and/or to surfaces in communities known as biofilms. Biofilm formation [1] facilitates
adherence to a variety of surfaces, including host tissues and abiotic surfaces such as medical implants, [2]
provides a reservoir from which bacteria can disperse to seed infections at other sites, and [3] imparts protection
both via a self-produced extracellular matrix comprised of polysaccharides and other macromolecules and by the
cells being physiologically distinct from each other and from free-living, planktonic cells. As a result, human
infections that involve a biofilm remain challenging to treat. Thus, understanding how bacteria form and disperse
from biofilms in the context of an animal is a critical area of research. While numerous models exist, few provide
all the advantages found with the symbiosis between the bacterium Vibrio fischeri and its squid host (Euprymna
scolopes), in which successful colonization depends on both biofilm formation and dispersal. Using this model,
we can [1] visualize the biofilms formed by V. fischeri on the surface of the symbiotic (light) organ and from
which it must disperse to enter to colonize spaces deep inside, [2] quantify the resulting colonization outcome,
and [3] evaluate roles of specific genes and assess gene expression in situ. Our work has shown that the
underlying mechanisms determined in the lab are also at play in the animal. We have found that both host-
associated biofilm formation and colonization depends on the production by V. fischeri of a matrix comprised of
SYP polysaccharide. Strains that fail to produce it fail to form symbiotic biofilms and are defective at colonizing
while those with an enhanced ability to produce this SYP-dependent matrix are superior in their ability to do
both. We have identified syp, an 18-gene locus required for production of SYP, multiple regulators that control
syp transcription and post-transcriptional events, and signals that activate or prevent SYP production. We have
determined that a large adhesive protein, LapV, is critical for production of SYP-dependent biofilms; dispersal
requires that LapV is cleaved from the cell surface. We have also identified additional biofilm and/or dispersal
factors whose roles are currently under investigation. We propose here to address key questions that will advance
our understanding of animal-relevant biofilm formation and dispersal, including when and where is SYP
produced during colonization? Is it shed upon dispersal? How and where do the signals that are known to control
SYP production function in the context of host colonization? How do specific regulators and signals function to
control biofilm formation and/or dispersal? Are the underlying mechanisms common to different isolates...

## Key facts

- **NIH application ID:** 10765411
- **Project number:** 2R35GM130355-06
- **Recipient organization:** LOYOLA UNIVERSITY CHICAGO
- **Principal Investigator:** Karen L Visick
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $432,426
- **Award type:** 2
- **Project period:** 2019-05-01 → 2029-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10765411

## Citation

> US National Institutes of Health, RePORTER application 10765411, Host-associated biofilm formation and dispersal mechanisms (2R35GM130355-06). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10765411. Licensed CC0.

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