# Host-associated biofilm formation and dispersal mechanisms

> **NIH NIH R35** · LOYOLA UNIVERSITY CHICAGO · 2021 · $384,792

## Abstract

Abstract
Bacteria can form multi-cellular communities in which individual cells are protected from environmental
insults such as antibiotics by virtue of being [1] encased in a protective matrix comprised of polysaccharides
and other macromolecules and [2] physiologically distinct from free-living, planktonic cells. Biofilm formation
enhances the ability of bacteria to colonize surfaces, including host tissues and abiotic surfaces such as medical
implants, and seeds subsequent infections at distal locations through dispersal processes. As a result of these
characteristics, bacteria in biofilms are responsible for the majority of hospital-acquired infections and thus
understanding how biofilms form and disperse from such biofilms is critical. Although numerous animal
models of biofilm formation have been developed, few, if any, permit visual examination of biofilm formation
and dispersal events as well as a quantitative analysis of subsequent colonization outcomes. One such robust
model, however, can be found in the Vibrio fischeri-squid (Euprymna scolopes) symbiosis. To colonize, V.
fischeri first forms a biofilm on the surface of the symbiotic organ, then disperses from it to enter and
ultimately colonize sites deep within this organ. Our work has shown that genes required for biofilm formation
in laboratory culture are similarly required for host-associated (HA) biofilms and colonization, while genetic
changes that enhance biofilm formation in the lab also strikingly enhance HA biofilms and colonization. This
strong correlation affords us an exceptional opportunity to develop and test hypotheses about the mechanisms
of HA-biofilms, dispersal and subsequent colonization. Our work has revealed that HA biofilms and
colonization depend on syp, an 18-gene locus involved in production of SYP polysaccharide, and on multiple
sensor kinases and response regulators that control syp transcription and post-transcriptional events. We have
recently identified calcium (Ca2+) and nitric oxide (NO) as a strong inducer and inhibitor, respectively, of
biofilm formation. Ca2+ is a physiologically relevant signal that appears to affect numerous processes, but how
it does so is as-yet unknown. NO, which is produced by the squid and known to influence HA-biofilms, likely
impacts one of the sensor kinases required for syp transcription, and we propose to evaluate the underlying
mechanisms. We are also poised to identify other physiological signals that promote/inhibit HA biofilms. We
have recently uncovered conditions in which dispersal can be visualized in laboratory culture, and have
observed that V. fischeri undergoes multiple rounds of formation and dispersal in fully-grown cultures, a result
that suggests control by post-transcriptional mechanisms. We have begun to investigate that process by
identifying a set of genes involved in controlling dispersal. We propose to develop a mechanistic understanding
of these dispersal genes and the factors that control dispers...

## Key facts

- **NIH application ID:** 10146420
- **Project number:** 5R35GM130355-03
- **Recipient organization:** LOYOLA UNIVERSITY CHICAGO
- **Principal Investigator:** Karen L Visick
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $384,792
- **Award type:** 5
- **Project period:** 2019-05-01 → 2024-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10146420

## Citation

> US National Institutes of Health, RePORTER application 10146420, Host-associated biofilm formation and dispersal mechanisms (5R35GM130355-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10146420. Licensed CC0.

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