By Pesach Benson • September 17, 2026
Jerusalem, 17 September, 2026 (TPS-IL) — Some disease-causing E. coli bacteria can rapidly adapt to find new ways to cling to human cells after losing the system they normally use to attach, an Israeli-led study has found.
The discovery sheds light on how disease-causing bacteria can adapt when one of their key attachment mechanisms stops working. It also suggests that blocking an alternative attachment mechanism could eventually offer a new way to prevent some infections.
Most E. coli bacteria are harmless, but some strains can cause illnesses ranging from diarrhea to serious intestinal and urinary tract infections.
The study, led by PhD student Noam Yedidi and professors Ilan Rosenshine and Sigal Ben-Yehuda of the Hebrew University of Jerusalem, focused on a strain of E. coli called enteropathogenic Escherichia coli, or EPEC. The bacteria can cause severe diarrhea, particularly in young children, while persistent infections can interfere with normal growth and development.
To cause an intestinal infection, EPEC first has to solve a basic problem: It must remain attached to the gut instead of being swept away.
Many EPEC strains use tiny, hair-like structures to attach to cells lining the intestine. But so-called atypical EPEC strains lack this attachment system and have nevertheless continued to cause infections.
The researchers wanted to know how.
They recreated the problem in the laboratory, starting with bacteria that had lost their main ways of attaching to human cells. They repeatedly selected bacteria that were still able to stick to the cells.
After only four rounds, the bacteria had become dramatically better at holding on. In some cases, their ability to attach increased more than 100-fold.
Two Ways to Adapt
The bacteria adapted in two different ways.
Some became unusually long, giving them more surface area and allowing more of their small attachment structures to make contact with human cells. Others changed a protein called FimH, which sits at the end of one of those structures and acts somewhat like a microscopic grappling hook.
Small genetic changes to FimH made it grip human cells more tightly.
“It is like losing a hook and quickly learning to use another one,” Rosenshine said. “The bacteria do not need to invent an entirely new system. They can take a tool they already have and improve it.”
The researchers then examined 327 atypical EPEC strains isolated from patients to determine whether the same process was occurring naturally. About half carried changes in the *fimH* gene.
When the researchers recreated and tested many of those naturally occurring changes, several made the bacteria attach to human cells 10 to 100 times more strongly.
The stronger attachment also appeared to help the bacteria do more than remain in place. EPEC uses a specialized system to inject proteins into human cells, interfering with their normal functions. Bacteria that attached more strongly were better able to deliver these proteins.
The findings could eventually point to a different approach to treating some E. coli infections. Instead of focusing only on killing the bacteria, researchers could seek to prevent them from attaching to the intestine in the first place.
The findings could have practical implications for future drug development. By blocking FimH or other attachment mechanisms, researchers may be able to prevent some EPEC bacteria from establishing infections without directly killing them. Such an approach could complement conventional antibiotics.
The study was published in the peer-reviewed journal Gut Microbes.
