Although there is an abundance of researchers working on developing effective treatments for Crohn’s, it can be hard to keep up on all the different things that are currently being done. In attempt to make research more transparent for all, here’s a few recaps on what researchers are finding– right now.
Artificial sweetener could intensify symptoms in those with Crohn’s disease
The new findings, recently published in Inflammatory Bowel Diseases, revealed increases in the numbers of Proteobacteria, a large phylum [group] of microbes, in the intestines of mice drinking water supplemented with Splenda. Half of the mice studied, belonging to a genetic line that suffers a form of Crohn’s disease were more affected than the remaining half of mice, which belong to a healthy mouse line. Splenda produced intestinal overgrowth of E. coli (a member of the Proteobacteria group) and increased bacterial penetration into the gut wall, but only in Crohn’s disease-like mice.
The researchers also found that Splenda ingestion results in increased myeloperoxidase activity in the intestines of mice with the bowel disease, but not in the healthy mice. Myeloperoxidase is an enzyme in leukocytes (white blood cells) that is effective in killing various microorganisms. The inference is that the increased presence of E. coli intensified the myeloperoxidase activity in the bowel as the body sought to fight off the invader. The findings suggest that consumption of Splenda may increase myeloperoxidase production only in individuals with a pro-inflammatory predisposition, such as Crohn’s disease or other forms of inflammatory bowel disease patients. As part of this process, inflammation and its attendant consequences could exacerbate the symptoms of Crohn’s disease.
“Our findings suggest that patients with Crohn’s disease should think carefully about consuming Splenda or similar products containing sucralose and maltodextrin,” said the study’s lead author, Alex Rodriguez-Palacios, DVM, MSc, DVSc, PhD, assistant professor of medicine at Case Western Reserve School of Medicine. “Several studies have examined the ingredients found in this widely available product, separately. Here, we used Splenda as a means to test the combined effect of the commercial ingredients and used one of the best animal models of ileal Crohn’s disease.” This study demonstrates that the sweetener induces changes in gut bacteria and gut wall immune cell reactivity, which could result in inflammation or disease flare ups in susceptible people. On the other hand, the study suggests that individuals free of intestinal diseases may not need to be overly concerned.”
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Engineering the gut microbiome with ‘good’ bacteria may help treat Crohn’s disease
Penn Medicine researchers have singled out a bacterial enzyme behind an imbalance in the gut microbiome linked to Crohn’s disease. The new study, published online this week in Science Translational Medicine, suggests that wiping out a significant portion of the bacteria in the gut microbiome, and then re-introducing a certain type of “good” bacteria that lacks this enzyme, known as urease, may be an effective approach to better treat these diseases.
“Because it’s a single enzyme that is involved in this process, it might be a targetable solution,” said the study’s senior author, Gary D. Wu, MD, associate chief for research in the division of Gastroenterology at the Perelman School of Medicine at the University of Pennsylvania. “The idea would be that we could ‘engineer’ the composition of the microbiota in some way that lacks this particular one.”
An imbalance in the gut microbiome — more “bad” bacteria than “good” — is known as dysbiosis, which is caused by environmental stressors, such as intestinal inflammation, antibiotics, or diet. Gut dysbiosis is believed to fuel Crohn’s disease and other diseases, but the mechanisms behind that relationship is not fully understood by researchers looking to strike a healthier, bacterial balance for patients. Crohn’s disease is an inflammatory bowel disease that affects nearly one million children and adults in the United States.
In a series of human and mouse studies, the researchers discovered that a type of “bad” bacteria known as Proteobacteria feeding on urea, a waste product that can end up back in the colon, played an important role in the development of dysbiosis.
The “bad” bacteria, which harbor the urease enzyme, convert urea into ammonia (nitrogen metabolism), which is then reabsorbed by bacteria to make amino acids that are associated with dysbiosis in Crohn’s disease. “Good” bacteria may not respond in a similar manner, and thus may serve as a potential therapeutic approach to engineer the microbiome into a healthier state and treat disease.
“The study is important is because it shows that the movement of nitrogen into bacteria is an important process in the development of dysbiosis,” Wu said. “It also proves using a single enzyme can reconfigure the entire composition of the gut microbiota.”
Using this approach, in the current study, researchers showed that inoculating pre-treated mice with a single bacterial species, Escherichia coli, altered the gut microbiome in a significant way, depending on the presence of urease. Mice injected with urease-negative E. coli did not lead to dysbiosis, while mice with urease-positive E. coli did. The urease-positive E. coli also exacerbated colitis in the mice.
The research was conducted by Wu and colleagues from Penn Medicine and Children’s Hospital of Philadelphia (CHOP), under the PennCHOP Microbiome Program with funding from the Crohn’s and Colitis Foundation.
Similar to mice, treating five human subjects with the same two antibiotics and PEG also successfully reduced bacterial load in their intestinal tract by 100,000-fold, suggesting that it might be possible to engineer the composition of the gut microbiota in patients with inflammatory bowel disease.
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Dysfunctional gene may be culprit in some Crohn’s disease cases
Sundrud’s laboratory, from The Scripps Research Institute (TSRI), is working to understand the characteristics and functions of TH17 cells, a subset of immune cells that circulate throughout the body. These cells protect many types of tissues from infection, but they can also promote chronic inflammatory conditions like Crohn’s disease, which specifically targets the intestinal tract.
Knowing TH17 cells need to function in a variety of tissue environments throughout the body, Sundrud’s team wondered if and how these cells might use different tools to behave normally in one environment — or tissue — than they’d use in another. Perhaps activating one gene could be useful in the lungs, while activating another would be useful in the gut, the same way you might bring a bathing suit on a trip to Florida and a jacket if you’re headed to Canada.
This study built on previous research from the Sundrud lab, which showed that when TH17 cells entered the intestine in human tissue samples, they increased the expression of a gene called MDR1.
But MDR1 is only known to transport chemotherapeutic drugs out of tumor cells, so why would it be expressed in immune cells in the gut?
The new study suggests that MDR1 is responsible for protecting TH17 cells in the gut from bile acids — detergent-like molecules produced by the liver that break down fats. Normally, the liver secretes bile acids after we eat to aid digestion. As food moves through the digestive tract, these acids are reabsorbed when they reach the ileum — the final portion of the small intestine — and the site of ileal Crohn’s disease, the most common form of Crohn’s.
“T cells only see high levels of bile acids in the ileum. They know this, and they adapt once they get there,” says Sundrud.
This discovery led the researchers to identify a mechanism where ileal Crohn’s disease appears to be induced by bile acids when T cell adaptation does not occur the way it should. The team used a genetically modified mouse model to observe the expression and function of MDR1 in mice. They found that the gene’s expression increased when the cells entered the ileum. But, in mice where the gene couldn’t be activated in the gut, TH17 cells that were exposed to bile acids suffered severe oxidative stress. This stress caused the TH17 cells to become overactive, leading to Crohn’s disease-like intestinal inflammation in mice.
Using bile acid sequestrants, an FDA-approved class of drugs used in transplant patients that absorb bile acids like a sponge, scientists were able to restore normal T cell function in the ileum and attenuate Crohn’s disease in mice.
To establish the relevance of their findings, the team tested blood samples from healthy humans, as well as those with a variety of inflammatory bowel diseases, including Crohn’s. They found a subset of patients with Crohn’s disease had severely impaired MDR1 expression.
Not only does this suggest that the cause of Crohn’s disease in these patients may be oxidative stress due to dysfunctional MDR1, but that for the subset of patients with this dysfunction, bile acid sequestrants may be an effective treatment. Together with his collaborators, Sundrud hopes to fund a clinical study to test exactly that.
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Blood Test for Colitis Screening Using Infrared Technology Could Reduce Dependence on Colonoscopy, Study Finds
A fast, simple blood test for ulcerative colitis using infrared spectroscopy could provide a cheaper, less invasive alternative for screening compared to colonoscopy, which is now the predominant test, according to a study between the Department of Physics and Astronomy and the Institute for Biomedical Sciences at Georgia State University.
The researchers used Attenuated Total Reflectance Fourier Transform Infrared (ATR-FTIR) spectroscopy to examine the blood serum of mice with colitis and found nine absorption peaks that could be used to indicate the presence of the disease in the blood sample.
The findings, recently published in the Journal of Biophotonics, suggest a new testing procedure that could be developed to help doctors more easily screen patients for ulcerative colitis.
More than 1.6 million people in the United States suffer from inflammatory bowel disease, which includes ulcerative colitis and Crohn’s disease. Ulcerative colitis causes inflammation and ulcers in the lining of the large intestine. Adults 50 and older are expected to get a colonoscopy, a test that allows a doctor to look at the inner lining of the large intestine (rectum and colon), every five years or more frequently if abnormalities are found. The test can help find ulcers, colon polyps, tumors and other areas of inflammation or bleeding.
However, many people don’t like getting colonoscopies because the procedure is uncomfortable and requires them to fast an entire day and clean out their colon by drinking a liquid solution. Colonoscopies can also be costly because they require sedation and several medical personnel and have risks of complications. There remains a great need for simpler and cost-effective techniques to diagnose inflammatory bowel disease, according to Dr. A. G. Unil Perera, Regents’ Professor of Physics, and Dr. Didier Merlin, professor in the Institute for Biomedical Sciences.
“Colonoscopy is used as a screening technique, so even if you don’t know if a person has colitis or not, that’s currently the only way to clearly check and say they do,” Perera said. “We are not talking about replacing colonoscopy. We have shown that a minimally invasive blood test can tell if a patient has an indication of colitis. Then, doctors can perform a colonoscopy to see how far the disease has spread and whether there are signs of cancer.”
This blood test using infrared spectroscopy is much quicker, less invasive and much less expensive compared to colonoscopy. There are no risks, except a simple finger prick to get a blood sample, Perera said.
In this study, the researchers used two groups of mice with different types of colitis, chronic and acute. The mice with chronic colitis, the interleukin 10 (IL 10) mice, had a gene modification that allowed them to develop colitis. The mice with acute colitis, the Dextran Sodium Sulphate (DSS) mice, were administered DSS in their drinking water for seven days, and they developed colitis over time. The control group in the study was mice before they were fed DSS.
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