A “copper economy” helps fungi and bacteria build better biofilms
Scientists have discovered that two common human pathogens can work together by managing copper in their shared environment - a finding that could open new ways to break down stubborn mixed biofilms
University of Exeter
image:
Candida albicans and Staphylococcus aureus mixed biofilm.
view moreCredit: Christian Hacker, Orlando Ross and Seána Duggan, University of Exeter
Scientists have discovered that two common human pathogens can work together by managing copper in their shared environment - a finding that could open new ways to break down stubborn mixed biofilms.
The fungus Candida albicans and the bacterium Staphylococcus aureus are both major causes of human infection. They are also found together in complex infections, including wounds, bloodstream infections and infections linked to medical devices.
When microbes form biofilms, they grow as surface-attached communities that can be difficult to treat. Mixed fungal-bacterial biofilms are especially challenging because different organisms can protect or support one another, making infections harder to clear.
Now, researchers led by Dr Seána Duggan, from the University of Exeter’s MRC Centre for Medical Mycology, have discovered that copper plays a central role in this fungal-bacterial partnership. The study, supported by the NIHR Exeter Biomedical Research Centre, reveals what the team describes as a microbial “copper economy”, in which the fungus and bacterium handle copper in different but complementary ways.
Dr Duggan said: “We usually think about copper as something that can kill microbes, because high levels are toxic. Our study reveals something more nuanced. In these mixed biofilms, copper appears to act almost like a shared currency that helps two very different pathogens cooperate. When that copper balance is disturbed, the partnership collapses. That gives us a potential new way to think about targeting infections that are difficult to treat because they involve more than one type of microbe.”
The team grew C. albicans and S. aureus together under laboratory conditions designed to mimic the human body. They found that the two species formed larger and more active biofilms than either microbe alone. Protein analyses showed that C. albicans increased proteins involved in copper uptake, while S. aureus increased proteins linked to copper export and copper stress protection.
Changing copper availability disrupted this cooperation. Both excess copper and copper limitation weakened the mixed biofilm, showing that the community depends on a finely balanced copper environment.
Dr Duggan said: “The most striking thing was that the mixed biofilm was much more sensitive to copper disruption than either organism alone. That tells us we are not just looking at the biology of one pathogen or the other. We are looking at the biology of the relationship between them.”
The study also showed that copper shaped the physical structure of the biofilm, and early tests suggest that copper-based approaches could help break these microbial communities down.
Dr Duggan said: “Mixed infections are a major clinical challenge, yet we still know relatively little about the molecular mechanisms inside these communities. Our work shows that micronutrients such as copper might dictate whether pathogens compete, cooperate, or become harder to treat. If we can identify the conditions that make these microbial partnerships fail, we may be able to design better ways to break them apart.”
The study highlights the importance of looking beyond single-pathogen infections and considering the cooperative behaviours that can emerge when fungi and bacteria grow together.
The paper is titled “Copper Driven Mutualism of Candida albicans and Staphylococcus aureus Interkingdom Biofilms” and is published in Microbiology.
Journal
Microbiology
Method of Research
Experimental study
Subject of Research
Cells
Article Title
Copper Driven Mutualism of Candida albicans and Staphylococcus aureus Interkingdom Biofilms
Article Publication Date
26-Jun-2026
Teamwork: An unexpected strategy bacteria use to survive antibiotics
When bacteria are under antibiotic attack, it is not ‘every man for himself.’ Researchers at Baylor College of Medicine and colleagues from collaborating institutions have discovered that bacterial populations work as a team to survive antibiotics. The study, published in the journal Science, reveals that bacteria pool their resources, helping quiescent or dormant cells survive. The findings help explain why some bacteria are hard to eliminate and suggest potential future approaches to improve antibiotic effectiveness.
“Antibiotics are designed to kill bacteria or stop them from growing. Yet many times antibiotics leave behind a small group of survivors,” said co-corresponding and lead author Dr. Christophe Herman, professor of molecular and human genetics and of molecular virology and microbiology at Baylor. “These survivors are not genetically resistant; instead, they temporarily shut down certain parts of their metabolism, entering a dormant-like state that allows them to endure treatment and later regrow. Understanding how survivors form and remain is a major challenge in fighting persistent infections.”
Scientists have long known that bacteria can help each other resist antibiotics by sharing genes that provide antibiotic resistance. In the current study, Herman and his colleagues investigated whether bacteria also could directly share proteins, the molecular machines that do most of the work in cells. Previous studies had indicated that bacteria can share proteins, but the experimental evidence was not clear.
“To detect protein transfer, we designed a sensitive system using the bacterium Escherichia coli,” said first author Alice X. Wen, a Baylor McNair Scholar in the Medical Scientist Training Program (MD/PhD), working in the Herman lab. “We engineered one group of bacteria (donors) to make a special enzyme called Cre, and another group of the same bacteria (recipients) to contain a genetic “switch” that could only flip if Cre protein entered the recipient.”
The system revealed that when donor and recipient bacteria were grown together, protein transfer occurred but was rare under normal conditions. But when the bacteria were exposed to low, non-lethal levels of antibiotics, protein transfer increased by thousands of times.
“We then investigated how proteins were moving from one cell to another,” Wen said. “We found that the transfer still occurred when donor cells were removed, leaving behind only the liquid in which they had grown. This ruled out direct cell-to-cell contact and pointed to something released into the environment.”
By combining biochemical techniques and advanced microscopy, the team discovered that tiny structures called membrane vesicles transported the proteins. Vesicles look like tiny bubbles made of bacterial membrane that pinch off from cells and float freely.
Looking closer, the recipient cells showed strong signs of dormancy – these cells slowed down protein production, reduced their metabolism and activated genes associated with persistence, such as HipA. “Recipient cells with high HipA activity were more likely to take up protein-carrying vesicles and survive antibiotic treatment,” Wen said. “When HipA was removed, both protein uptake and survival dropped.”
Protein transfer also helped dormant bacteria survive exposure to lethal antibiotic doses after vesicle transfer; that is, exposing cells to an increased concentration of vesicles before antibiotic treatment led to increased survival. The results suggested that transferred proteins helped dormant cells endure stress while their own protein production was shut down.
“Our study shows that antibiotics cause a genetically identical group of bacteria to differentiate into two distinct groups: donor cells that respond by releasing protein-filled vesicles, and recipient cells that become dormant but capable of taking up proteins from incoming vesicles, which helps them survive,” Herman said. “This teamwork allows vulnerable members of a bacterial population to persist in the face of a potentially deadly antibiotic attack.”
The researchers are interested in identifying the proteins in vesicles that contribute to recipient persistence. Understanding donor-recipient interactions among bacteria opens new doors in the fight against chronic and persistent infections.
For a complete list of contributors to this work, their affiliations and financial support for the study, see the publication.
###
Journal
Science
Method of Research
Experimental study
Subject of Research
Cells
Article Title
Antibiotics stimulate protein transfer to persister cells
Article Publication Date
25-Jun-2026
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