Houston, TX - Jun 25, 2026

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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.