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Researchers discover the brain helps kill bacteria and boost antibiotics


It’s a well known fact that bacterial resistance to antibiotics has reached crisis levels, now a new breakthrough could give antibiotics a well needed boost.


It turns out that our brain might control much more than just our thoughts and physical actions. Announced this week a new study, from the Queen Mary University of London (QMUL), shows that it also controls how our body responds to bacterial infections by boosting the production of a protective molecule called PCTR1 that helps white blood cells kill the invading bacteria.


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Our body is in constant contact with bacteria, whether it’s alien bacteria that cause disease, or our own vital microbiome, and over the past decade, as many of these alien bacteria become increasingly resistant to antibiotics, so much so that the World Health Organisation believe that at least 10 million people a year could die because of it. As a consequence over the past few years there has been a flurry of research to find a new ways to tackle the problem of bacterial disease. One of the most promising methods at the moment could be CRISPR, a revolutionary gene editing technique, which is not only helping us to create new forms of life that are resistant to every known virus but also helping us create new genetic chainsaws that rip through bacterial cells.

In order to identify new, novel avenues to treat bacterial infections the team at QMUL turned their attention to the body’s Central Nervous System (CNS) – our brain, spinal cord and optic nerves – because in the past several studies have implicated the brain in orchestrating more than just our thoughts. During their study they found that severing the right vagus nerve in mice lead to a significant impairment in their ability to clear E. coli infections.

When the team investigated the reason for this, they found a significant decrease in the levels of a molecule called Protectin Conjugate in Tissue Regeneration 1 (PCTR1) which is part of a group of molecules called specialised pro-resolving mediators that control how our body responds to inflammation. PCTR1 is produced by white blood cells in the body from an essential fatty acid called docosahexaenoic acid.


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The team also found that the decrease in PCTR1 reduced the ability of macrophages, a type of white blood cell, to kill E. coli and then they investigated how the vagus nerve regulated PCTR1 production in the abdominal cavity of the mice, where this nerve is known to regulate white blood cell behaviour during inflammation they found that the nerve releases a neurotransmitter called acetylcholine which then instructs another type of immune cell – innate lymphoid cells – to increase production of PCTR1. This in turn regulated macrophages’ ability to find and kill bacteria.

When they injected the mice with the severed vagus nerve with PCTR1, they found that it restored the ability of peritoneal macrophages to get rid of the bacteria, as well as dampen the subsequent inflammatory response, accelerating the bacteria’s termination.

The results are expected to have wide ranging implications in the fight against bacterial infections, especially in light of the alarming rate at which bacteria are becoming resistant to antibiotics because the findings demonstrate that we can give our body a hand by using PCTR1, and related molecules, to enhance its ability to clear bacteria during infections – reducing our reliance on antibiotics.

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