Epidemiological studies have revealed a strong correlation between red meat consumption and the development of inflammatory bowel disease. In a new study published in Molecular Nutrition and Food Research that was conducted in mice, red meat consumption caused an imbalance of bacteria in the intestinal microbiota.
Investigators fed mice various kinds of red meat, including pork, beef, and mutton, for two weeks, and then they induced colitis with 2.5% dextran sulfate sodium. Intake of these three red meat diets exacerbated colonic inflammation. Analyses revealed an overproduction of pro-inflammatory cytokines and infiltration of immune cells in the colon of mice fed red meat diets.
These diets led to a marked decrease in the relative abundance of Streptococcus, Akkermansia, Faecalibacterium, and Lactococcus bacterial strains, coupled with an increase in Clostridium and Mucispirillum.
“This study contributes to improving food innervation approaches for inflammatory bowel disease treatment and indicates a close crosstalk among diet, gut microbiota, and intestinal immunity,” said co–corresponding author Dan Tian, MD, PhD, of Capital Medical University, in China.
Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health
About a dozen studies in the past five years have made claims linking nearly every type of human cancer with the presence of microbiomes, “communities” of bacteria, viruses and fungi that live in or on peoples’ bodies. Now, scientists at Johns Hopkins Medicine say a study that sequenced human cancers found far less microbial DNA sequences than earlier studies reported in the same cancer tissue samples.
“It’s the nature of science to validate, confirm and reproduce findings,” says Steven Salzberg, PhD, Professor of Biomedical Engineering, Computer Science, and Biostatistics at The Johns Hopkins University. “Over time, we see a more complete picture of new research, and in this case, we did not find any associations between microbiomes and many types of cancer.”
Salzberg says details of the new study, published Sept. 3 in Science Translational Medicine, surveyed the whole genome sequences generated from 5734 tissue samples collected from 25 cancer types and stored in a large National Cancer Institute-funded database, The Cancer Genome Atlas (TCGA). About half of the samples are from normal tissues and blood, the other half from solid tumours and blood-based cancers.
The TCGA’s whole genome sequencing data contains millions of chopped up pieces of DNA molecules, known as reads, from each tissue sample. The original goal of the TCGA studies was to identify mutations in the DNA sequence of genes that might be associated with various cancer types. Sometimes, though, the original tumors might have microbes in them, and the reads could be used to identify those microbes.
Because reads often contain contaminants from bits of DNA left behind in sequencing machinery or picked up from the air or surfaces, samples can acquire DNA from those sources, as well as from the original tumour tissues. Salzberg says extraordinary efforts were made to identify such contaminants, preventing their study from displaying false results.
To rule out contaminants, Salzberg and his team relied on extensive experience with genomic sequencing and careful analysis of control samples to identify reads belonging to sequences known or highly likely to have contaminated samples.
For the current study, a continuation of one that the Johns Hopkins team published in 2023, Salzberg and first author Yuchen “Peter” Ge, a graduate student in biomedical engineering at Johns Hopkins, removed human DNA sequences from the TCGA data sets by mapping each read against two human reference genomes – one from the Telomere-to-Telomere (T2T) project and another from the Genome Reference Consortium.
After removing human DNA, the research team was left with, on average, 2.4 million reads per sample, or about 0.35% of the total 6.5 billion tumour sample reads. Of these, the research team found 323 million human DNA reads that weren’t eliminated in the first pass and 986 million reads they classified as contaminants.
They next compared the remaining sequencing reads against a database containing 50 651 genomes representing 30,355 species of bacteria, viruses, fungi and archaea (single-celled organisms that aren’t bacteria or viruses).
After removing human DNA sequences and contaminants, the average proportion of microbial DNA reads in solid tumour samples was 0.57% and 0.73% in blood cancers.
The Johns Hopkins researchers then compared their new results to a study published five years ago in the journal Nature [since retracted, because of concerns about contaminants in the microbial data], and found the previous study identified 56 times as many microbial reads as the new study for half of the total microbial reads. And 5% of the time, the previous study found 9,000 times the number of microbial reads as the current Johns Hopkins study. Salzberg says the microbial reads in the retracted study were highly likely to be contaminants.
“This disparity in the number of microbial reads didn’t occur in just a few samples,” says Salzberg. “Over the whole study, the previous researchers found far more microbial reads than we did.”
In another comparison of a study published in Cell in 2022 and the current Johns Hopkins work, the 2022 study reported fungal DNA amounts that were hundreds of times more than what was found in the current Johns Hopkins study, largely due to contaminants.
Among the DNA samples in the current Johns Hopkins study, in which they did find microbiome DNA, the researchers found microbes that have long been linked with human cancer, such as HPV (linked with cervical and some head and neck cancers), Helicobacter pylori (linked to stomach cancer), and Fusobacterium nucleatum and Bacteroides fragilis (linked with GI cancers).
The current Johns Hopkins study and the previous ones published in Cell and Nature reported microbiomes of Saccharomyces cerevisiae, commonly known as baker’s yeast. “It’s one of the most common contaminants in sequencing labs,” says Salzberg. They also found a virus that infects plant fungi, Rosellinia necatrix partitivirus 8, which has no known link to human disease.
Salzberg said the need to carefully document claims about the links between cancer and microbiomes is “especially important” as efforts ramp up to diagnose cancers early using microbiome information.
The Johns Hopkins researchers have made their sequencing analysis data available online to other scientists in the supplementary materials in Science Translational Medicine and online.
New study supports anecdotal claims about the risks of using a smartphone during toilet time
Photo by Jan Antonin Kolar on Unsplash
Survey participants who reported using a smartphone while on the toilet had a higher risk of haemorrhoids than non-users. Chethan Ramprasad of Beth Israel Deaconess Medical Center, U.S., and colleagues present these findings in a new study in the open-access journal PLOS One on September 3, 2025.
Every year in the US, haemorrhoids lead to nearly 4 million visits to the doctor or emergency room and more than $800 million in healthcare spending. Haemorrhoids involve swollen veins in the anal or rectal area and can cause pain and bleeding. Anecdotal evidence has linked smartphone use on the toilet with increased risk of haemorrhoids.
However, few studies have explored whether smartphone use on the toilet is actually associated with haemorrhoid risk. To help clarify, Ramprasad and colleagues conducted a study of 125 adults undergoing screening colonoscopy. The participants answered online survey questions about their lifestyle and toilet habits, and endoscopists evaluated them for haemorrhoids.
Among all participants, 66% reported using smartphones on the toilet, and they tended to be younger than non-users. After statistically accounting for other factors thought to possibly be linked with haemorrhoid risk – such as exercise habits, age, and fibre intake – the researchers found that participants who used a smartphone on the toilet had a 46% higher risk of haemorrhoids than non-users.
Time spent on the toilet was significantly higher for smartphone users than non-users; 37% of smartphone users spent more than 5 minutes at a time on the toilet compared to just 7.1% of non-users. Reading news and using social media were the most commonly reported smartphone activities on the toilet. Interestingly, straining while using the toilet was not associated with increased haemorrhoid risk, in contrast to some prior studies.
On the basis of the findings, the researchers suggest that smartphone use may inadvertently prolong toilet time, potentially increasing pressure in anal tissues, which may then lead to haemorrhoids.
This study could help inform clinicians’ recommendations to patients. Future research could also expand on these findings, such as by tracking patients over time and exploring interventions to limit prolonged smartphone use on the toilet.
Trisha Pasricha, senior author of the study, adds: “Using a smartphone while on the toilet was linked to a 46 per cent increased chance of having haemorrhoids. We’re still uncovering the many ways smartphones and our modern way of life impact our health. It’s possible that how and where we use them – such as while in the bathroom –can have unintended consequences.
“This study bolsters advice to people in general to leave the smartphones outside the bathroom and to try to spend no more than a few minutes to have a bowel movement. If it’s taking longer, ask yourself why. Was it because having a bowel movement was really so difficult, or was it because my focus was elsewhere?
“It’s incredibly easy to lose track of time when we’re scrolling on our smartphones – popular apps are designed entirely for that purpose. But it’s possible that constantly sitting longer on the toilet than you intended because you’re distracted by your smartphone could increase your risk of haemorrhoids. We need to study this further, but it’s a safe suggestion to leave the smartphone outside the bathroom when you need to have a bowel movement.”
Rates of inflammatory bowel disease are rising, and there’s currently no cure. IBD can also be deadly: up to 8% of people with the disease develop blood clots, which can lead to heart attack and stroke. New research has uncovered why blood clotting malfunctions in IBD – and identified drugs that normalise blood clotting in human cells and animal models of IBD.
“We think we can leverage these findings to reduce inflammation and the risk of blood clots,” says senior author Aaron Petrey, PhD, assistant professor of microbiology and immunology at University of Utah Health, associate director of the U’s Molecular Medicine Program. “This could be lifesaving.”
Most research into IBD has focused on immune cells. But blood cells called platelets are another key contributor to IBD symptoms. In healthy people, platelets clump together into clots in response to injuries to stop bleeding, and don’t form clots otherwise. But in patients with IBD, platelets are on a hair trigger, ready to form clots at the slightest provocation.
Surprisingly, platelets from IBD patients weren’t clotting via the normal pathways that trigger clotting, says first author Rebecca Mellema, PhD, pathology postdoc. “It’s completely independent of what we would expect.”
“There’s an innate mechanism by blood vessels to tell platelets to stay quiet and not form a clot yet,” Petrey explains. “Once there’s injury or inflammation, that signal can switch over and tell them to form a clot. That’s the process that’s broken in IBD patients.”
IBD platelets appear to clot more often because they don’t have enough of a key protein called layilin, the researchers found. In healthy people, layilin acts as a molecular brake for clotting: it senses the difference between healthy and injured blood vessels and prevents platelets from clotting as long as blood vessels are intact.
But when the researchers deleted the layilin gene in mice, the brakes came off. Without layilin, platelets were extra sticky, forming clots when they shouldn’t.
The researchers also found that platelets from IBD patients only had about 60% of the layilin protein that they should, leaving them constantly on the verge of clotting.
A promising drug target
Layilin prevents unwanted clotting by tamping down the activity of a clot-triggering molecule called Rac1. In mice without the layilin gene – and in people with IBD – Rac1 is always a little bit too active, which means platelets are too prone to forming clots.
But there’s good news. Drugs that prevent Rac1 activity are already in clinical trials for other conditions, and the researchers’ results suggest that these Rac1 inhibitors could be powerful therapeutics for IBD.
One Rac1 inhibitor reduced excessive clotting in human platelets in a dish. The inhibitor also decreased the level of tissue damage in the gut in a mouse model of IBD.
Promisingly, the drug decreased clotting in platelets from IBD patients even more strongly than it affected healthy cells. “We have shown a hyperactivation pathway in resting IBD patient platelets, but they’re also incredibly sensitive to treatment, moreso than those from a healthy person,” Mellema says.
Normalizing Rac1 activity might not only reduce the risk of heart attack and stroke—it could also help alleviate day-to-day IBD symptoms, the researchers say. Excessive clotting can block blood flow in the gut and make inflammation worse, which means that preventing clotting could reduce inflammation.
Unlike established anti-clotting drugs, the researchers say, Rac1 inhibitors shouldn’t lead to an increased risk of dangerous bleeding, which is a serious concern for IBD patients with chronic inflammation. Blocking Rac1 won’t interfere with other, independent pathways that can trigger platelet clotting, so the cells should still be able to form needed clots in response to injury.
“We’re targeting a pathway that is not pre-activated in healthy people,” Petrey says. “So we can address that step of the pathway, and if there’s a significant injury, the platelets can overcome that inhibition.”
Other groups had been looking into the potential of Rac1 inhibitors to reduce inflammation in IBD. The new work emphasises the potential of these drugs to address multiple symptoms. “Paying more attention to what we can do to address these blood clotting risks could significantly improve patient lives,” Petrey says.
Crohn’s disease, a debilitating inflammatory bowel disease, has many known contributing factors, including bacterial changes in the microbiome that foster an inflammatory environment. Now, for the first time, Crohn’s disease has been tied to a virus – specifically, Epstein-Barr virus (EBV), best known for causing infectious mononucleosis (mono).
Researchers had already observed increased levels of EBV in the intestine of patients with Crohn’s disease and had also found associations between EBV and autoimmune diseases other than Crohn’s, including lupus, multiple sclerosis, and rheumatoid arthritis.
Nandy and colleagues analyzed data from a cohort of initially healthy military recruits, aged 20 to 24, who provided periodic serum samples throughout their service. They tested the samples with VirScan, a high-throughput assay developed by study coauthor Stephen Elledge, PhD, at Harvard Medical School. VirScan enables detection of antibodies against a wide range of viruses, providing insights into viral exposures.
Compared with healthy controls, military personnel whose samples were positive for anti-EBV antibodies were three times more likely to eventually develop Crohn’s disease. Interestingly, evidence of EBV exposure preceded their Crohn’s diagnosis by five to seven years.
“We went into this study not looking for EBV; we were looking for any virus that might elicit inflammatory bowel disease,” says Scott Snapper, MD, PhD, the study’s senior investigator and director of the Inflammatory Bowel Disease Center at Boston Children’s. “Then, when EBV was a hit, we looked very specifically at immune responses to EBV with more detailed tests.”
These tests bore out and strengthened the VirScan findings.
The team next looked for anti-EBV antibodies in a second cohort – more than 5000 children (median age; 11 years) who were first-degree relatives of people with Crohn’s disease. In this cohort, EBV was not a statistically significant predictor of a subsequent Crohn’s disease diagnosis. Snapper speculates that having first-degree relatives with Crohn’s could already have put them at increased risk due to shared genetic or environmental factors, muddying the association with EBV.
EBV and the immune system
Another possibility is that EBV affects children’s immune systems differently, perhaps because children are less likely to develop infectious mono when exposed. “Responding to certain organisms early in life may boost the immune system in a way that prevents immune-mediated disease,” Snapper says.
Nandy and Snapper now want to figure out what EBV does to people at a molecular level to make them more susceptible to Crohn’s disease.
One possibility is that the virus has certain genes or molecules that interact with human genes involved in susceptibility to autoimmune conditions. Another may relate to an anti-inflammatory protein produced by EBV, remarkably similar to mammalian IL-10. People exposed to that protein may make antibodies against it, preventing their own IL-10 from working and leaving them susceptible to inflammatory disease.
“Mechanistically, we need to understand exactly how EBV alters the immune system leading to Crohn’s disease,” Snapper says. “If you could figure out the mechanisms, you could come up with new therapies.”
A large prospective study published in Molecular Nutrition and Food Research reveals that a healthy plant-based diet is linked with a reduced risk of inflammatory bowel disease (IBD).
For the study, 143 434 individuals in the UK reported on their dietary intake. During an average follow-up of 14.5 years, 1117 participants developed inflammatory bowel disease – 795 cases of ulcerative colitis and 322 cases of Crohn’s disease.
A healthy plant-based diet was associated with an 8% lower risk of ulcerative colitis, and a 14% lower risk of Crohn’s disease. An unhealthy plant-based diet was associated with a 15% higher risk of Crohn’s disease, with results suggesting that this was in part due to higher intake of vegetable oils and animal fats. Fruits and vegetables were identified as protective factors against inflammatory bowel disease.
Blood analyses suggested that the benefits seen in this study might be explained by the anti-inflammatory properties of plant-based foods.
“Our research indicates that a healthy plant-based diet may protect against inflammatory bowel disease, with its anti-inflammatory properties playing a key role,” said corresponding author Zhe Shen, MD, of the Zhejiang University School of Medicine, in China.
New research in rats indicates that a Mediterranean plant may be an effective treatment for ulcerative colitis, a type of inflammatory bowel disease. The findings are published in the Journal of the Science of Food and Agriculture.
Various antioxidant and anti-inflammatory medications are used to treat ulcerative colitis, but they can cause numerous side effects. To test the potential of the Arbutus unedo plant (often referred to as the strawberry tree) that is native to the Mediterranean region, investigators gave rats doses of an extract from the plant before exposing the animals to acetic acid, a chemical that induces ulcerative colitis.
The pretreatment prevented changes in the colon’s lining and led to fewer colonic lesions compared with no pretreatment. The pretreatment also caused decreased expression of various proteins that promote oxidative stress and inflammation.
“Our findings suggest that Arbutus unedo should be studied further in preventative and therapeutic approaches to gastrointestinal disorders,” said corresponding author Soumaya Wahabi, PhD, of the University of Jendouba, in Tunisia.
A study led by biomedical scientists at the University of California, Riverside School of Medicine shows how a genetic mutation associated with Crohn’s disease can worsen iron deficiency and anaemia — one of the most common complications experienced by patients with inflammatory bowel disease, or IBD. The research is published in the International Journal of Molecular Sciences.
While IBD — a group of chronic inflammatory disorders that includes Crohn’s disease and ulcerative colitis — primarily affects the intestines, it can have effects beyond the gut. Iron deficient anaemia is the most prevalent of these effects, contributing to chronic fatigue and reduced quality of life, particularly during disease flare-ups.
The study, performed on serum samples from IBD patients, reports that patients carrying a loss-of-function mutation in the gene PTPN2 (protein tyrosine phosphatase non-receptor type 2) exhibit significant disruption in blood proteins that regulate iron levels. This mutation is found in 14-16% of the general population and 19-20% of the IBD population. A loss-of-function mutation is a genetic change that reduces or eliminates the normal function of a gene or its product, a protein.
“This discovery sheds light on a critical mechanism that links a patient’s genetics to their ability to absorb and regulate iron, which is essential for maintaining healthy blood and energy levels,” said Declan McCole, a professor of biomedical sciences at UCR who led the study. “Our findings offer an explanation for why some IBD patients remain iron-deficient despite oral supplementation.”
When the researchers deleted the PTPN2 gene in mice, the animals developed anaemia and were unable to absorb iron effectively. The team found this was due to reduced levels of a key iron-absorbing protein located in the intestinal epithelial cells — the cells responsible for taking up dietary nutrients.
“The only way the body can obtain iron is through intestinal absorption from food, making this discovery particularly significant,” said first author Hillmin Lei, a doctoral student in McCole’s lab. “Disruption of this pathway by genetic variants like those in PTPN2 could help explain why some IBD patients fail to respond to oral iron therapy, a commonly prescribed treatment for anaemia.”
McCole stressed that the study is a vital step toward understanding how genetic risk factors for IBD can compound patient symptoms by interfering with nutrient absorption.
“It opens new avenues for targeted therapies that go beyond inflammation control to address systemic complications like anaemia,” he said. “This includes prioritising patients who carry loss-of-function PTPN2 variants to be treated for anaemia with systemic intravenous iron supplementation rather than oral iron, which may be poorly absorbed.”
The study, , was performed in collaboration with researchers at the City of Hope, University Hospital Zurich, and the Swiss IBD Cohort.
Microscopic colitis (MC) is a chronic inflammatory bowel disease that severely reduces quality of life. MC is responsible for over 30% of all chronic diarrhoea cases in people over 65 years of age, and its prevalence is rising worldwide. Although little is known about what causes MC, previous studies have suggested that a range of common medications could trigger the condition, including non-steroidal anti-inflammatory drugs (NSAIDs), blood pressure medications, and selective serotonin reuptake inhibitors (SSRIs).
However, according to a new large-scale, longitudinal study of older adults in Sweden from Mass General Brigham, Broad Institute of MIT and Harvard, and Karolinska Institutet researchers, most of these medications are not associated with increased risk of MC. Results are published in Annals of Internal Medicine.
“Our study demonstrated that, contrary to the previous belief, it’s unlikely that medications are the primary triggers for microscopic colitis,” said corresponding author Hamed Khalili, MD MPH, associate director of the Clinical and Translational Epidemiology Unit and director of Clinical Research at the Crohn’s and Colitis Center at Massachusetts General Hospital, a founding member of the Mass General Brigham health care system. “Clinicians should carefully balance the intended benefits of these medications against the very low likelihood that they cause microscopic colitis.”
To look for associations between medication use and MC diagnosis, the researchers analyzed data for over 2.8 million individuals aged 65 years and older in Sweden. The data included information on prescribed medications, hospitalizations, medical diagnoses, and gastrointestinal biopsy results.
Overall, they found that the risk of developing MC was less than 0.5%. There was no association between NSAIDs, angiotensin converting enzyme (ACE-I) inhibitors, angiotensin II receptor blockers (ARBs), proton pump inhibitors (PPIs), or statins and the risk of developing MC, but individuals prescribed SSRIs had a 0.04% higher risk of developing MC. However, the researchers also showed that individuals prescribed SSRIs were also more likely to receive a colonoscopy, which is necessary to diagnose MC.
“Our analyses suggest that surveillance bias is a likely explanation for earlier findings that implicated medications in the pathogenesis of microscopic colitis and may also explain the continued association with SSRIs,” said senior author Jonas F. Ludvigsson, MD PhD, paediatrician at Örebro University Hospital and Professor at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet in Sweden.
The study did not include data on primary care visits, which could impact the likelihood of colonoscopy, or lifestyle factors such as diet and smoking status.
Chronic inflammatory bowel disease is challenging to treat and carries a risk of complications, including the development of bowel cancer. Young people are particularly affected: when genetic predisposition and certain factors coincide, diseases such as ulcerative colitis or Crohn’s disease usually manifest between the ages of 15 and 29 – a critical period for education and early career development. Prompt diagnosis and treatment are crucial. Researchers at Charité – Universitätsmedizin Berlin have now discovered a therapeutic target that significantly contributes to halting the ongoing inflammatory processes. Their findings are published in the current issue of the journal Nature Immunology*.
Sometimes gradually, sometimes in flare-ups – accompanied by severe abdominal cramps, diarrhoea, weight loss, fatigue and a high level of emotional stress – this is how the two most common chronic inflammatory bowel diseases, Crohn’s disease and ulcerative colitis, often begin. While ulcerative colitis only affects the inner lining of the large intestine, Crohn’s disease can involve the entire thickness of the intestinal wall, most commonly in the small intestine, but sometimes also the stomach and oesophagus. Ongoing inflammation can cause lasting tissue damage and increase the risk of cancer. While traditional treatments aim to suppress the immune system as a whole, newer therapies are more targeted: they interrupt the inflammatory process by blocking specific messenger substances that drive inflammation in the body.
The exact causes of severe systemic diseases are still not fully understood. In addition to genetic factors, environmental influences are also believed to play an important role in their development. Prof Ahmed Hegazy has been studying inflammatory processes in the gut and the immune system’s defence mechanisms at Charité’s Department of Gastroenterology, Infectiology and Rheumatology for several years. Together with his team, he has now succeeded in identifying the interaction between two messenger substances of the immune system as the driving force behind chronic intestinal inflammation: Interleukin-22, a protein that supports the cells lining the inside of the gut and helps maintain the protective barrier, and oncostatin M, a signalling molecule that plays a significant role in tissue repair and cell differentiation.
Uncontrolled chain reaction
“At the clinic, we mainly see young patients who just beginning their professional lives. So far, we have only been able to slow down the progression of the disease and alleviate symptoms. But not all patients respond well to existing treatments, so new therapeutic approaches are urgently needed,” says Ahmed Hegazy. In previous work, the research team closely examined the effects of oncostatin M, an inflammation-promoting messenger molecule. This protein, produced by certain immune cells, activates other inflammatory factors – setting off a chain reaction that triggers an excessive immune response. “It was especially interesting for us to see that patients with high levels of oncostatin M do not respond to several common therapies,” Ahmed Hegazy explains. “This means that Oncostatin M levels could help predict treatment failure and may serve as a biomarker for more severe disease. That’s exactly where we focused our efforts: we wanted to understand this signaling pathway better and find ways to block it with targeted treatments.”
The research team spent five years uncovering how the immune messenger oncostatin M triggers inflammatory responses. They began by using animal models, and later studies tissue samples from patients, to examine the different stages of chronic intestinal diseases, State-of-the-art single-cell sequencing showed that – compared to healthy tissue – a much larger number of unexpected cell types in the inflamed gut have receptors for oncostatin M. At the same time, additional immune cells start producing the inflammatory protein. Interestingly, interleukin-22, which normally protects tissue, also makes the gut lining more sensitive to oncostatin M by increasing the number of its receptors. “These two immune messengers work together and amplify the inflammation, drawing more immune cells into the intestine, like a fire that keeps getting more fuel and spreads,” as Ahmed Hegazy relates. “In our models, we specifically blocked the binding sites for oncostatin M and saw a clear reduction in both chronic inflammation and the associated of cancer.”
Targeted therapy for high-risk patients in sight
The researchers found a particularly high number of receptors for the messenger molecule oncostatin M around the tumours in tissue samples from patients with colorectal cancer caused by chronic intestinal inflammation, but not in the surrounding healthy tissue. This observation suggests that this signalling pathway may help promote cancer development. But chronic inflammation does not always lead to bowel cancer, and not every patient is affected in the same way, making treatment and prognosis difficult. With an understanding of oncostatin M’s amplifying effect on interleukin-22, new therapies may be possible.
The team’s experimental findings may soon translate into a real-world therapy: by specifically disrupting the harmful interaction between the immune messengers interleukin-22 and oncostatin M. “Our results provide a strong scientific basis for developing targeted treatments against this inflammation-promoting mechanism in chronic inflammatory bowel disease — particularly in patients with more severe forms of the illness,” explains Ahmed Hegazy. A clinical trial is already underway to test an antibody that blocks the receptors for Oncostatin M.
