A study published in the journal Science on June 25, 2026, reports that bacterial populations share proteins to help dormant cells survive antibiotic treatment. Researchers from Baylor College of Medicine conducted the study.

Christophe Herman, a professor of molecular and human genetics and of molecular virology and microbiology at Baylor College of Medicine, said, "Antibiotics are designed to kill bacteria or stop them from growing. Yet many times antibiotics leave behind a small group of survivors." He added, "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." Herman stated, "Understanding how survivors form and remain is a major challenge in fighting persistent infections."

The research involved using the bacterium Escherichia coli to detect protein transfer between donor and recipient bacterial groups. Alice X. Wen, first author and Baylor McNair Scholar in the Medical Scientist Training Program, said, "To detect protein transfer, we designed a sensitive system using the bacterium Escherichia coli." She explained, "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."

Protein transfer between bacteria was rare under normal conditions but increased by thousands of times when exposed to low, non-lethal levels of antibiotics. The study found that membrane vesicles, which are tiny structures made of bacterial membrane, transported the proteins between cells. Wen said, "We found that the transfer still occurred when donor cells were removed, leaving behind only the liquid in which they had grown." She added, "This ruled out direct cell-to-cell contact and pointed to something released into the environment."

Recipient cells that took up protein-carrying vesicles showed signs of dormancy, including slowed protein production, reduced metabolism, and activation of persistence-associated genes such as HipA. Wen said, "Recipient cells with high HipA activity were more likely to take up protein-carrying vesicles and survive antibiotic treatment." She noted, "When HipA was removed, both protein uptake and survival dropped." Exposing cells to an increased concentration of vesicles before antibiotic treatment led to increased survival against lethal antibiotic doses.

Herman said, "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." He added, "This teamwork allows vulnerable members of a bacterial population to persist in the face of a potentially deadly antibiotic attack."