Scientists from Trinity College Dublin (TCD) have made a breakthrough that could lead to improved treatment options for tuberculosis (TB) in the future.

TB is an infection caused by a bacterium called Mycobacterium tuberculosis. Despite being one of the oldest known diseases, it remains the world's deadliest infectious disease, and is very common in parts of the world such as Africa.

While it is much less common in developed countries, including Ireland, the growing problem of antibiotic resistance poses a major healthcare threat worldwide.

Part of the reason why TB is such a successful pathogen is because it is able to infect the cells of the immune system, which are normally tasked with responding to infections. It infects the lung macrophage cells and then manipulates them to its benefit, creating a safe home for it to hide out undisturbed, sometimes for years.

However, scientists at TCD have discovered how TB puts the brakes on our immune engines, and how we can kick start these engines to work again.

They had been examining how lung macrophage immune cells fuel the fight against infection. This work has been at the forefront of showing how the simple sugar, glucose, is used to promote the macrophages anti-bacterial activities.

The scientists found that persistent infection of these macrophages with TB puts the brakes on the glucose-filled engine. This, in effect, shuts down the body's natural response to infection, allowing the bacteria to hide undisturbed.

Specifically, Dr Emer Hackett of the TCD team found a small RNA molecule, which is made up of tiny pieces of genetic information, which the bacteria promotes and which targets key enzymes that act as pumps in our immune engines to commit glucose to promote the anti-bacterial response.

When the bacteria promotes this small RNA molecule, known as microRNA-21, these enzyme pumps are removed from the engine and glucose is not used in the same way. This then allows the bacteria to escape and thrive.

However, the study also offers some hope for the future.

"We found that when TB-infected cells are treated with a key ‘interferon gamma protein signal', which is normally produced following vaccination, they will remove this microRNA to effectively relieve the brake and restore our normal immune response," explained Dr Frederick Sheedy of TCD.

He insisted that this could have major implications for the future treatment of TB.

"What is particularly promising from a societal impact perspective is that as well as increasing our knowledge of how TB corrupts our normal immune response to infection, our identification of the microRNA-21 means that scientists should be able to develop improved immunotherapies or vaccine strategies to help in the fight against TB infection," Dr Sheedy said.

Details of the scientists' findings are published in the journal, Cell Reports.