The treatment of chronic inflammatory bowel diseases has long been a challenge, particularly in young patients where disease manifestation often coincides with critical periods of education and early career development. Prompt diagnosis and treatment are crucial to prevent complications, including the development of bowel cancer. Researchers at Charité – Universitätsmedizin Berlin have made a groundbreaking discovery that significantly contributes to halting ongoing inflammatory processes, published in Nature Immunology.

Crohn’s disease and ulcerative colitis, the two most common chronic inflammatory bowel diseases, can be debilitating and life-altering. While traditional treatments focus on suppressing the immune system as a whole, newer therapies aim to interrupt the inflammatory process by blocking specific messenger substances that drive inflammation in the body.

Prof. Ahmed Hegazy has been studying inflammatory processes in the gut and the immune system’s defense mechanisms for several years. He has identified the interaction between two immune messenger substances – interleukin-22 and oncostatin M – as the driving force behind chronic intestinal inflammation. This uncontrolled chain reaction amplifies inflammation, drawing more immune cells into the intestine like a fire that spreads.

The research team spent five years uncovering how the immune messenger oncostatin M triggers inflammatory responses. They used animal models and examined tissue samples from patients to study the different stages of chronic intestinal diseases. State-of-the-art single-cell sequencing showed that in inflamed gut tissue, there are many unexpected cell types with binding sites for oncostatin M.

Interestingly, interleukin-22 normally protects tissue but also makes the gut lining more sensitive to oncostatin M by increasing its receptors. This interaction between the two immune messengers works together and amplifies inflammation, much like a fire getting more fuel and spreading.

In their models, the researchers specifically blocked the binding sites for oncostatin M and saw a clear reduction in both chronic inflammation and cancer associated with it. The team’s experimental findings may soon translate into real-world therapy by disrupting the harmful interaction between interleukin-22 and oncostatin M.

A clinical trial is already underway to test an antibody that blocks the receptors for oncostatin M. This targeted treatment has the potential to revolutionize the management of chronic inflammatory bowel diseases, particularly in patients with more severe forms of the illness. The discovery offers a new era in chronic inflammation treatment, providing hope for those affected by these debilitating conditions.

A recent study by researchers at WEHI in Melbourne, Australia has made groundbreaking discoveries about how our daily food choices can rapidly impact our gut health. The pre-clinical study revealed that even a few meals high in saturated fats can cause inflammation in the body, despite physical symptoms potentially taking years to appear.

The research found that the gut protective protein, IL-22, was rapidly depleted in mice after just two days of eating high-fat foods. This is a significant breakthrough that could help pinpoint how chronic inflammation occurs at its source.

Chronic inflammatory diseases, such as coeliac disease, inflammatory bowel disease, and rheumatoid arthritis, affect about one in three Australians. However, the exact mechanism behind this inflammation remains largely unknown. The study’s findings suggest that our daily food choices can have an immediate effect on our gut health, paving the way for future interventions to boost gut health and tackle chronic inflammation.

Researchers also discovered that short-term exposure to high-fat diets can reduce the production of IL-22, a crucial protein that helps control gut inflammation. This is the first time the rapid impact of high-fat diets on this protein has been shown.

The study’s findings have significant implications for our understanding of how chronic inflammation arises and causes disease. By highlighting the importance of incorporating unsaturated fats into our diets to naturally boost gut protection, researchers hope their findings will influence dietary guidelines and promote better nutrition-based strategies for people at risk of chronic inflammatory diseases.

In summary, this research demonstrates the rapid impact of fatty meals on gut defenses and suggests that our daily food choices can have a significant effect on our gut health. The study’s findings could lead to new methods to restore or boost gut function for people living with chronic inflammatory diseases.

The relationship between obesity and diabetes has long been a subject of scientific interest. Researchers at Tohoku University Graduate School of Medicine have made a groundbreaking discovery that sheds light on the missing link between these two conditions. Their study reveals that colonic inflammation, triggered by obesity, plays a crucial role in regulating glucose homeostasis through the hepatic ERK pathway.

Insulin is a hormone produced by β-cells in the pancreas that unlocks cells to let glucose enter from the blood. However, individuals with obesity often become insulin-resistant, causing their pancreas to secrete more insulin to try and keep up. This study shows that inflammation in the colon, triggered by obesity, activates the ERK pathway in the liver, which stimulates the neuronal relay pathway and increases β-cell production.

The researchers conducted a series of experiments on mice to determine if colonic inflammation due to obesity could impact the hepatic ERK pathway. They found that causing inflammation in the colon activated the ERK pathway in the liver, stimulated the neuronal relay pathway, and increased β-cells even in mice without obesity. By analyzing colons of mice with induced obesity, they also found that colonic inflammation had occurred along with both hepatic ERK pathway activation and increased β-cells.

Moreover, when the researchers treated obese mice with colon inflammation by lowering their inflammation, it actually stopped the ERK pathway in the liver from activating. This exciting finding suggests that targeting colon inflammation could be a potential way to prevent or treat diabetes.

This research has significant implications for understanding the mechanism behind β-cell proliferation and maintaining normal blood glucose levels. It is anticipated that these findings will lead to advancements in developing treatments and prevention methods for diabetes, ultimately improving the lives of millions of people worldwide.

The study was published in JCI Insight on May 8, 2025, and was supported by various grants from the Japan Society of the Promotion of Science (JSPS), Japan Science and Technology Agency (JST), and Japan Agency for Medical Research and Development (AMED).