An Early Marker of Inflammatory Bowel Disease - European Medical Journal

An Early Marker of Inflammatory Bowel Disease

2 Mins

CELL COMMUNICATION has been shown to be a contributing factor to intestinal inflammation, according to work carried out by scientists at Michigan State University, East Lansing, Michigan, USA. More specifically, the results highlighted the pathogenic relationship between gut sensory neurons and enteric glia, providing a potential treatment target for gastrointestinal inflammatory diseases.

Approximately 11% of the world’s population are affected by inflammatory bowel disease and irritable bowel syndrome. One way to combat the rising number of patients affected by these diseases is early detection of the disorders; however, the difficulty with studying inflammatory bowel diseases is that the number of cell–cell interactions and signalling cascades means any attempt to map the interactions has more connections than a spider’s web. The study’s senior author, Dr Brian Gulbransen, Michigan State University, explained: “The enteric nervous system is an exceedingly complex network of neural circuits that programmes a diverse array of gut patterns and is responsible for controlling most gastrointestinal functions.”

By investigating specific molecular changes in early inflammation, the researchers identified tachykinins as one of the key markers that preclude a patient’s earliest feelings of discomfort. These proteins, derived from enteric neurons, drive neuroinflammation of the gut through multicellular signalling cascades of enteric neurons, nerve fibres, and enteric glia.

The researchers then aimed to determine a treatment target within this signalling cascade by identifying a promotor of inflammation. One protein of interest was NK2R, a receptor crucial to neurone–glial communication. The blocking of NK2R with GR 159897, a known inhibitor of the receptor, inhibited signalling between the glial and neuronal cells. This disconnection in communication had beneficial effects on disease recovery: “It [GR 159897] proved to be quite effective in accelerating recovery from inflammation,” stated Dr Gulbransen.

Although the authors recognise that this research requires further work, with a number of genes and proteins yet to be investigated or fully understood, this study marks a landmark in the battle against debilitating inflammatory bowel diseases, with hope that this discovery will pave the way towards the development of new therapeutic techniques.

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