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Itzik Bellenitzki/TPS-IL on 1 March, 2020
Hebrew University Researchers Discover How E. coli Outsmarts Human Cells
Jerusalem, 5 April, 2026 (TPS-IL) -- Researchers at the Hebrew University of Jerusalem have discovered a two-part mechanism used by a pathogenic strain of E. coli to weaken the human immune response, demonstrating how a single bacterial protein can both suppress alarm signals inside cells and prevent the cell from regaining control. The peer-reviewed study, published in Advanced Science, focused on enteropathogenic Escherichia coli (EPEC), a bacterium that causes intestinal infections. EPEC employs a molecular injection system to deliver proteins directly into human cells, where they alter cellular processes to aid the invading pathogen.
The researchers discovered that one such protein, NleD, operates with greater precision than previously thought. NleD was already known to disable immune signaling by cutting intracellular molecules that enable cells to detect infection and activate a defense response. The new research demonstrates that the same protein also targets a regulator that helps manage that signaling network.
Instead of destroying the regulator, NleD binds to it and blocks its function, preventing it from interacting with its normal cellular targets. According to the researchers, this gives the bacterium a dual advantage: it weakens the initial immune response and also disrupts the system that would normally help the cell rebalance those signals. The study was led by Dr. Yaakov Socol with Professors Sigal Ben-Yehuda, Yael Litvak, and Ilan Rosenshine of the Hebrew University, in collaboration with Professor J. Sivaraman of the National University of Singapore.
The findings enhance scientists’ understanding of how bacterial pathogens manipulate host cells during infection. The researchers stated that this work could also influence future treatment strategies, especially as antibiotic resistance increases interest in alternatives to conventional drugs.
One such approach is to target specific interactions between bacterial proteins and human cells, rather than merely killing the bacteria themselves. The study also offers new insights into how immune signaling pathways function under normal conditions and are disrupted during infection.
