Featured Article 15 Sep 2017
Researcher working with fungi on a plate. Image: Tonhom1009/Shutterstock
Researcher working with fungi on a plate. Image: Tonhom1009/Shutterstock

As recently as July, the World Health Organisation (WHO) warned of an urgent demand for new antibiotics after the discovery of a strain of gonorrhoea that could survive any medication used to treat it.

Now, a team from Trinity College Dublin (TCD) is hoping to aid this effort after finding a way to look into the very heart of some of the most common disease-causing bacteria and help find ways to treat them.

In a paper published to Nature Communications, the team led by Prof Martin Caffrey revealed it used x-ray crystallography techniques to ‘look under the bacterial bonnet’ and produce a molecular blueprint.

The blueprint could be used to design drugs that minimise off-target effects and attack any of their structural weaknesses.

One of the key findings was that two common, potentially deadly bacteria – Pseudomonas aeruginosa and Escherichia coli ­– share a remarkably similar structure, but differ in the finer detail.
“These subtle differences might be exploited to design species-specific therapies with a reduced likelihood for the development of antibiotic resistance,” said Caffrey.

The challenges

From a medical perspective, discovering these nuances is crucial because not only do they cause problems in tens of thousands of patients every year, but they have also developed a resistance to a multitude of drugs.

This means new methods are badly needed to treat them, but even with the latest blueprint of the bacterial enzyme ‘Lnt’, creating effective candidates is no easy feat.

This is because the new drug would need to be specific to only affect the bacterial enzyme in humans and not other animals. Also, targeting the bacteria might result in the unwanted slowing of the body’s natural response to infection.

Speaking of where the research goes from here, Caffrey said: “The structural blueprints generated as part of this study provide a basis whereby the differences between the bacterial enzyme and the immune response proteins might be exploited, with the goal of producing a drug that only hits the bacterial target.”

Colm Gorey

This article originally appeared on www.siliconrepublic.com and can be found at:

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