Study may lead to new strategies to combat bacterial infection

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February 26, 2017 01:14
1 minute read.
A sample bottle containing E. coli bacteria is seen at the Health Protection Agency in north London

A sample bottle containing E. coli bacteria is seen at the Health Protection Agency in north London. (photo credit: REUTERS)

Infectious bacteria in contaminated food that can cause deadly diarrhea in children or intestinal tract conditions in adults around the world are smarter than we thought.

Hebrew University researchers have discovered how these pathogens exploit our cells and colonize our gut.

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Enteropathogenic bacteria kill over 2 million infants each year in developing countries alone. The infection process involves hundreds of genes and proteins, both in the infectious bacteria and the human host. But the processes by which the bacteria establish themselves the gut has been poorly understood.

Now, a study led by led by bacteriology Prof. Ilan Rosenshine of HU’s medical faculty and published in Science describes how pathogens sense their host and tailor their gene expression to trigger disease.

These findings could lead to new strategies to combat bacterial infection.

Working with a pathogenic strain of E. coli, the researchers found that the bacteria can sense attachment to the human intestinal cells and activate gene expression in response.

This was shown by engineering one of these genes to express a protein that stains the expressing bacteria to appear green under the microscope. Under microscopic examination, the researchers observed that only the attached bacteria fluoresce in bright green, while non-attached bacteria remain dark.



The researchers also deciphered how – upon sensing that it has attached to intestinal cells – the pathogen reorganizes its gene expression, including genes involved in virulence and metabolism to exploit the host cell.

“The next steps include mapping in detail the genes that change their expression upon attachment, and describing the precise effects of this expression remodeling,” said Rosenshine. “Another important issue is testing whether similar regulation is involved in the infection processes of other pathogens.”


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