Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

A new study led by researchers at the Kennedy Institute and published today in Immunity sheds light on the drivers behind Inflammatory bowel disease (IBD) and suggests potential new targets for treatment of the condition.

 

IBD is a long-term disease involving inflammation of the gut and affecting around 260 000 in the UK. The term usually refers to two conditions – ulcerative colitis and Crohn's disease.

The exact causes of IBD are not yet known, but it is widely accepted that a combination of genetic factors and disruptions to the immune system play a central role in the condition.

The Kennedy researchers showed that the production of eosinophils – a type of white blood cell present in the immune system – is higher in colitis, as is the accumulation of substances linked to eosinophils in the inflamed intestine. The team led by Prof Fiona Powrie and Dr Thibault Griseri also found that eosinophils release toxic and inflammatory substances during colitis, highlighting their potential for causing disease.

Whilst eosinophils are commonly associated with beneficial immune responses against parasites they are also linked to harmful allergic responses. Although they are quite abundant in the healthy intestine, their role in the gut immune stability is enigmatic and the molecular signals that drive them from protective to tissue damaging are unknown.

Identifying the molecular mechanisms causing IBD is key to developing new treatments for the condition, and in this study Dr Griseri and team were able to identify the inflammatory molecule - the cytokine GM-CSF - as a crucial driver of the pathogenic activity of eosinophils in colitis.

"We are enthusiastic about these data as we think that together with our former study revealing a key role for GM-CSF in dysregulated white blood cell production in the bone marrow during colitis, our study highlights GM-CSF as a key driver of chronic inflammation and a potential novel therapeutic target in IBD", says Dr Thibault Griseri.

Read full paper at Immunity.

 

Image: Microscopic view of eosinophil granulocyte, component of the white blood cells or leukocytes of the immune system having cytoplasmic granules, showing the lobed nucleus; Somersault1824/Shutterstock.com.

Similar stories

NIHR Fellowships awarded to NDORMS researchers

Congratulations to Eileen Morrow and Mae Chester-Jones who have received NIHR Doctoral Fellowships

ORUK Early Career Research Fellowship awarded to NDORMS researcher

Congratulations to Jack Tu who has been awarded an Orthopaedic Research UK Early Career Research Fellowship to explore the cause of knee pain after total knee replacement.

OCTRU - delivering answers to important clinical questions

The Oxford Clinical Trials Research Unit (OCTRU) has received NIHR benchmarking results and offers excellent value for money according to the report

Unhelpful thoughts about fracture symptoms hinder recovery

The importance of mindsets and feelings about fracture symptoms have been shown to be a key factor in recovery of musculoskeletal conditions.

Fat tissues can play a protective role against inflammation in the intestine

A new study in The EMBO Journal has revealed how fat tissues might provide a protective role in intestinal inflammation opening new lines of research into the treatment of inflammatory bowel diseases.

NDORMS researchers awarded Sir Henry Wellcome Fellowships

Kennedy Institute researchers Mariana Borsa and Edward Jenkins have both been awarded Sir Henry Wellcome Postdoctoral Fellowships, which give recently qualified postdoctoral researchers the opportunity to start independent research careers.