If your teeth have ever felt fuzzy after skipping a brushing, you’ve encountered biofilm—a slimy bacterial layer that clings to surfaces. In medical settings, biofilms make infections harder to treat when they form protective shields for bacteria on devices like catheters and implants.
UC Riverside scientists have now discovered a chemical that plants produce when they're stressed prevents biofilm from forming. The breakthrough offers potential advances in healthcare as well as preventing equipment corrosion in industrial settings.
“In simple terms, biofilms are communities of microorganisms, like bacteria or fungi, that stick together and form a protective layer on surfaces,” said Katayoon Dehesh, distinguished professor of molecular biochemistry at UCR, and corresponding author of a study about the discovery.
“You’ve probably seen them as the slimy layer on river rocks or the plaque on your teeth. While they’re a natural part of many ecosystems, biofilms can cause big problems.”
The study, published in the journal Nature Communications, highlights the importance of a particular metabolite, which is a molecule produced during life-sustaining chemical reactions inside plants, as well as bacteria and even some parasites, like the one that causes malaria.
In plants, this metabolite, MEcPP, plays a critical role not only in producing essential compounds but also in stress signaling. For example, when a plant is damaged in some way and too much oxygen enters its cells, it accumulates MEcPP. This molecule then triggers protective responses within the plant. The researchers discovered that this same molecule has a surprising effect on bacteria like E. coli: it disrupts biofilm development by interfering with its ability to attach to surfaces.
In medical settings, biofilms grow on devices like catheters, stents, or implants, making infections harder to treat because the microbes in biofilms are highly resistant to antibiotics. In industrial contexts, they clog pipes, contaminate food processing equipment, and cause corrosion.
“By preventing the early stages of biofilm development, this molecule offers real potential to improve outcomes in any industries reliant on clean surfaces,” Dehesh said.
Bacteria rely on hair-like structures called fimbriae to anchor themselves to surfaces, a critical step in biofilm initiation. Fimbriae help bacteria latch onto medical implants, pipes, or even teeth, where they secrete a protective matrix that shields them from antibiotics and cleaning agents. Without fimbriae, biofilm formation cannot begin.
“Biofilms are like fortresses for bacteria,” said Jingzhe Guo, UCR project scientist and first author of the paper. “By disrupting the initial phase of attachment, MEcPP essentially disarms the bacteria’s ability to establish these fortresses.”
Through genetic screenings of more than 9,000 bacterial mutants, the research team identified a key gene called fimE, which acts as an "off switch" for fimbriae production. MEcPP enhances the activity of this gene and increases the expression of fimE. This, in turn, prevents the bacteria from producing fimbriae and forming biofilms.
“Our discovery could inspire biofilm prevention strategies across a wide range of industries,” Guo said. “From cleaner water systems to better dental care products, the possibilities are immense.”
Biofilms are not only a medical concern but also a costly problem in industrial settings. They contribute to clogged pipelines, corroded machinery, and contamination in food processing facilities. Traditional methods for managing biofilms often rely on harsh chemicals or expensive treatments, which can be harmful to the environment or ineffective over time as bacteria adapt.
“This study is a testament to the unexpected connections between plant biology and microbiology,” Guo said. “It’s thrilling to think a molecule that plants use to signal stress might one day help humans combat bacterial threats.”
Journal
Nature Communications
Article Title
An evolutionarily conserved metabolite inhibits biofilm formation in Escherichia coli K-12
Article Publication Date
21-Nov-2024