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Medscape
18-07-2025
- Health
- Medscape
Dietary Emulsifiers and Their Role in IBD
WASHINGTON, DC — A low-emulsifier-containing diet led to a threefold increased likelihood of improvement in symptoms of Crohn's disease compared with an emulsifier-containing diet in a randomized double-blind dietary trial involving 154 patients with mildly active disease living across the United Kingdom. The findings were reported at Gut Microbiota for Health (GMFH) World Summit 2025 by Benoit Chassaing, PhD, of the Institut Pasteur, Paris, France, whose research leading up to the trial has demonstrated that food additive emulsifiers —ubiquitous in processed foods — alter microbiota composition and lead to microbiota encroachment into the mucus layer of the gut and subsequent chronic gut inflammation. Patients in the ADDapt trial, which was also reported in an abstract earlier this year at the European Crohn's and Colitis Organization (ECCO) 2025 Congress, had a Crohn's disease activity index (CDAI) of 150-250 and evidence of inflammation (faecal calprotectin (FCP) ≥ 150 µg/g or endoscopy/radiology). All 'had been exposed in their regular diets to emulsifiers,' said Chassaing, a co-investigator, during a GMFH session on 'Dietary Drivers of Health and Disease.' They were randomized to either a low-emulsifier diet or to a low-emulsifier diet followed by emulsifier 'resupplementation' — a design meant to 'account for the very strong placebo effect that is always observed with dietary studies,' he said. All patients received dietary counseling, a smart phone app and barcode scan to support shopping, and weekly support. They also received supermarket foods for 25% of their needs that were either free of emulsifiers or contained emulsifiers, and they were provided three snacks per day that were emulsifier-free or contained carrageenan, carboxymethycellulse (CMC), and polysorbate-80 (P80) — dietary emulsifiers that are commonly added to processed foods to enhance texture and extend shelf-life. In the intention-to-treat (ITT) analysis, 49% of patients in the intervention group reached the primary endpoint of a 70-point reduction or more in CDAI response after 8 weeks compared with 31% of those in the control group ( P = .019), with an adjusted relative risk of response of 3.1 ( P = .003), Chassaing shared at the GMFH meeting, convened by the American Gastroenterological Association and the European Society of Neurogastroenterology and Motility. In the per-protocol analysis (n = 119), 61% and 47% of patients in the intervention and control groups, respectively, reached the primary outcome of CDAI response, with an adjusted relative risk of response of 3.0 ( P = .018), he said. Secondary endpoints included CDAI remission at 24 weeks, and according to the abstract for the ECCO Congress, in the ITT analysis, patients in the intervention group were more than twice as likely to experience remission. Chassaing noted at the GMFH meeting that as part of the study, he and coinvestigators have been investigating the participants' gut microbiota with metagenomic analyses. The study was led by Kevin Whelan, head of the Department of Nutritional Sciences at King's College London, London, England. Can Emulsifier-Sensitive Individuals Be Identified? In murine model research 10 years ago, Chassaing showed that the administration of CMC and P80 results in microbiota encroachment into the mucus layer of the gut, alterations in microbiota composition — including an increase in bacteria that produce pro-inflammatory flagellin — and development of chronic inflammation. Wild-type mice treated with these compounds developed metabolic disease, and mice that were modified to be predisposed to colitis had a higher incidence of robust colitis. Moreover, fecal transplantation from emulsifier-treated mice to germ-free mice reproduced these changes, 'clearly suggesting that the microbiome itself is sufficient to drive chronic inflammation,' he said. In recent years, in humans, analyses from the large French NutriNet-Sante prospective cohort study have shown associations between exposure to food additive emulsifiers and the risk for cardiovascular disease, the risk for cancer (overall, breast, and prostate), and the risk for type 2 diabetes. But to explore causality and better understand the mechanisms of emulsifier-driven changes on the microbiota, Chassaing and his colleagues also launched the FRESH study (Functional Research on Emulsifier in Humans), a double-blind randomized controlled-feeding study of the emulsifier CMC. For 11 days, nine healthy patients consumed an emulsifier-free diet and 11 consumed an identical diet enriched with 15 g/d of CMC. Patients on the CMC-containing diet had reduced microbiota diversity and depletions of an array of microbiota-related metabolites, but only a small subset had profound alterations in microbiota composition and increased microbiota encroachment into the mucus layer. 'Some seemed to be resistant to CMC-induced microbiota encroachment, while some were highly susceptible,' Chassaing said. The pilot study raised the question, he said, of whether there is an 'infectivity component' — some kind of 'sensitive' gut microbiota composition — that may be associated with dietary emulsifier-driven inflammation and disease. In other murine research, Chassaing and his team found that germ-free mice colonized with Crohn's disease-associated adherent-invasive E coli (AIEC) and subsequently given CMC or P80 developed chronic inflammation and metabolic dysregulation, 'clearly demonstrating that you can convert resistant mice to sensitive mice just by adding one bacteria to the ecosystem,' he said. 'The presence of AIEC alone was sufficient to drive the detrimental effects of dietary emulsifiers.' (In vitro research with transcriptomic analysis then showed that the emulsifiers directly elicit AIEC virulence gene expression, Chassaing and his coauthors wrote in their 2020 paper, facilitating AIEC's 'penetration of the mucus layer and adherence to epithelial cells and resulting in activation of host pro-inflammatory signaling.') 'We don't think it's solely the AIEC bacteria that will drive emulsifier sensitivity, though…we think it's more complex,' Chassaing said at the meeting. Overall, the findings raise the question of whether emulsifier-sensitive individuals can be identified. This, he said, is one of his most recent research questions. His lab has led the development of an in vitro microbiota model built to predict an individual's sensitivity to emulsifiers. In a study published in April, the model recapitulated the differential CMC sensitivity observed in the earlier FRESH study, suggesting that an individual's sensitivity to emulsifiers can indeed be predicted by examining their baseline microbiota. Interpreting the Epidemiology Chassaing's research arch illustrates the synergy between epidemiological research, basic/translational research, and clinical interventional research that's needed to understand the diet-microbiome intersection in inflammatory bowel disease, said Ashwin Ananthakrishnan, MBBS, MPH, associate professor of medicine at Massachusetts General Hospital, Boston, in an interview at the meeting. 'It's a good example of how to really span the spectrum, starting from the big picture and going deeper to understand mechanisms, and starting from mechanisms and expanding it out,' Ananthakrishnan said. In his own talk about research on IBD, Ananthakrishnan said that epidemiological data have shown over the past 10-15 years that total dietary fiber is inversely associated with the risk for Crohn's disease (with the strongest associations with fiber from fruits and vegetables). Studies have also shown that a higher intake of polyunsaturated fatty acids is associated with a lower risk for ulcerative colitis, whereas 'an n-6-fatty acid-rich diet is associated with a higher risk of ulcerative colitis,' he said. Dietary cohort studies, meanwhile, have shed light on the influence of dietary patterns — such as the Mediterranean diet and diets with high inflammatory potential—on IBD. A diet rich in ultra-processed foods has also been shown in a prospective cohort study to be associated with a higher risk for Crohn's disease, with certain categories of ultra-processed foods (eg, breads and breakfast foods) having the strongest associations. Such studies are limited in part, however, by inadequate assessment of potentially relevant variables such as emulsifiers, preservatives, and how the food is processed, he said. And in interpreting the epidemiological research on fiber and IBD, for instance, one must appreciate that 'there are a number of mechanisms by which fiber is impactful…there's a big picture to look at,' Ananthakrishnan said. Fiber 'can affect the microbiome, clearly, it can affect the gut barrier, and it can affect bile acids, and there are detailed translational studies in support of each of these.' But there are other constituents of fruits and vegetables 'that could potentially influence disease risk, such as AhR ligands and polyphenols,' he said. 'And importantly, people not eating a lot of fiber may be eating a lot of ultra-processed foods.' Most interventional studies of fiber have not shown a benefit of a high-fiber diet, Ananthakrishnan said, but there are multiple possible reasons and factors at play, including potential population differences (eg, in inflammatory status or baseline microbiota), shortcomings of the interventions, and potentially inaccurate outcomes. Abigail Johnson, PhD, RDN, associate director of the Nutrition Coordinating Center, University of Minnesota Twin Cities, which supports dietary analysis, said during the session that the focus of dietary research is 'moving toward understanding overall dietary patterns' as opposed to focusing more narrowly on vitamins, minerals, and macronutrients such as proteins, fats, and carbohydrates. This is an improvement, though 'we still don't have good approaches for understanding [the contributions of] things like additives and emulsifiers, food preparation and cooking, and food processing,' said Johnson, assistant professor in the Division of Epidemiology and Community Health at University of Minnesota Twin Cities. 'Perhaps by looking at things at the food level we can overcome some of these limitations.'
Local France
10-07-2025
- Health
- Local France
'The risk is real': France sees rise in cases of chikungunya fever
So far this year, mainland France has recorded 25 ' cas autochtones ' - or locally-transmitted cases of the disease, found in people who have not travelled to an area where the infection is common, out of 761 total cases. Doctors in France have warned of the risks of the virus, which causes fever and joint point and can in rare cases lead to more serious complications. Deaths are rare in countries that have access to good healthcare facilities. Chikungunya is generally described as a tropical disease and is common in Africa, Asia, the Caribbean and the Pacific Islands. It can, however, be spread by the bite of tiger mosquito - an Asian import that is now commonly found throughout southern and central France, and as far north as Paris. READ ALSO : MAP: Tiger mosquitoes reach northern France✎ The French Indian Ocean island of La Réunion is currently in the grip of a chikungunya epidemic that has caused 200,000 cases of the virus and 20 deaths since the start of the year. Advertisement Experts at the public health body Santé Public France say that while most of the cases in mainland France are in people who have recently travelled to La Réunion - or other areas where chikungunya is common - a rising number of cases are being diagnosed in people who have not recently left France. Cases have been recorded in Corsica and the southern Provence-Alpes-Côte d'Azur region before, but this year has also seen a case in the cooler, northern region of Grand Est. Anna-Bella Failloux, an entomologist at the Institut Pasteur, told France Info : "Such an early start to the mosquito's activity season and such a high number of cases had never been observed before. "We didn't expect to detect a locally transmitted case in the Grand Est." Eric d'Ortenzio, an epidemiologist at the Inserm institute, added: "The risk is real. "We need to monitor the situation and tell the population to protect themselves, by using mosquito repellents - the only means of preventing this disease." Since May 1st, Santé Publique France has been tracking cases of the virus, especially those that are the result of local transmission. "For the time being, the situation is not worrying, but we must remain vigilant," said Anna-Bella Failloux. What is chikungunya and how to protect against it? The virus is spread by the bites of infected mosquitoes, especially the tiger mosquito. Symptoms start four to eight days after the bite and include fever, joint and muscle pain, headache, nausea and fatigue. Most people will recover without treatment within a week, but complications can occur, especially in people who have ongoing health conditions. Advertisement There is no specific treatment for chikungunya. A vaccine does exist, but it has been linked with various side effects, and as a result French health authorities are no longer recommending it for the general population - anyone in a high-risk group should speak to their doctor. The best way to prevent it is to avoid mosquito bites by wearing mosquito repellent during the summer months - tiger mosquitoes (the smaller, black and white striped ones) are active throughout the day. They are found in almost all of France apart from the northern coast. READ ALSO : How to prevent the spread of tiger mosquitoes in France✎
Yahoo
02-07-2025
- Business
- Yahoo
IntegraGen: Sales of €2.5 Million in the First Half of 2025 and Cash Position of €2.1 Million
Sequencing activities at Évry down 31% Decrease in activities on the P2M microbiology platform operated on the Institut Pasteur site Free cash position of €2.1m at June 30, 2025, after a consumption of €0.9m in the first half. The cash situation at this rate of consumption may not allow the company to continue its activities without new financing beyond the first quarter of 2026 EVRY, France, July 02, 2025--(BUSINESS WIRE)--Regulatory News: IntegraGen (FR0010908723 – ALINT – Eligible PEA PME), an OncoDNA company specializing in the genomics of cancer and rare genetic diseases, which performs interpretable genomic analyses for academic and private laboratories, announces today its unaudited sales for the first half of 2024. Sales for the first half came to €2,540K, down 34% compared with the first half of 2024 on a like-for-like basis (excluding revenues from the SeqOIA platform), contrary to expectations of weak growth, comparable to that of 2024, as announced by the Company in its press release dated April 29, 2025, on its results for the 2024 financial year. This decline is the result of reduced activity of over 40% on the Institut Pasteur's Mutualized Microbiology platform, linked to the drop in epidemiological sequencing, as well as to the decline in projects carried out on the Evry genomics platform, down by around 31%. This decline is the result of delays in the start-up of two major projects, the first samples of which were received by the company in May, as well as a general slowdown in research projects for academic and hospital customers. The company believes that the second half of the year, with the acceleration of major projects (notably UMBRELLA) and improved funding conditions for public research, should enable the situation to improve from the third quarter onwards. As of June 30th, available cash, including the remainder on the loan granted to the parent company OncoDNA and repaid over the course of 2025, stood at €2.1m. The company used up €0.9m of cash in the first half of 2025, and at this rate may not have enough cash to ensure its financing for the next 12 months. In this context, the company is exploring all strategic options to improve its situation and expects to reduce cash consumption in the second half of the year through the reduction of operating costs, the launch of services for several existing customers, external sources of financing, a resumption of customer research projects, as well as the expected upturn in customers' research budgets. Given the high level of uncertainty surrounding public research funding, the Company is not maintaining its revenue growth forecasts for 2025. Bernard Courtieu, Chief Executive Officer of IntegraGen, comments: "The first half of the year has been extremely difficult, with both a sharp drop in academic and hospital research projects, linked to a reduction in public research financing, as well as a reduction in the budgets of several biotech companies in a sector affected by the general economic climate. Despite several successes such as the UMBRELLA project, whose operational launch was announced last month, IntegraGen needs to find new sources of funding to be able to ensure the continuity of its operations." Investors are invited to carefully read section 4.2 of the 2024 Management Report on "Principal risks and uncertainties facing the Company". Financial results for the first half of 2025 will be published in October. ABOUT INTEGRAGEN IntegraGen is an OncoDNA group company specializing in the genomics of cancer and rare genetic diseases. Backed by highly competent and qualified teams, IntegraGen is a leading player in DNA sequencing services and genomic data interpretation software. The company runs one of the largest NGS labs in France and operates for research institutes of excellence. As part of OncoDNA group, IntegraGen leverages the power of next generation sequencing with the mission of delivering the promise of precision medicine to patients. IntegraGen has about 40 employees and generated €8.5 million of turnover in 2024. Based in France, IntegraGen is part of the Belgian OncoDNA group present in Spain, UK, Germany and works with an international network of 35 distributors. The Group also provides biomarker testing and clinical interpretation tools to guide treatment and monitoring of late stage solid tumors and accelerate the development of new cancer drugs. IntegraGen is listed on Euronext Growth in Paris (ISIN: FR0010908723 – Mnemo: ALINT – Eligible PEA- PME). View source version on Contacts IntegraGen Bernard COURTIEUDirecteur GénéralVirginie De CosterDirecteur Administratif et Financiercontact@ Tél. : +33 (0)1 60 91 09 00 NewCap Relations Investisseurs Louis-Victor DELOUVRIERintegragen@ Tél. : +33 (0)1 44 71 98 53 Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
Gizmodo
05-06-2025
- Health
- Gizmodo
This Genetic ‘Trick' Helped the Black Death Linger for Centuries
Yersinia pestis—the bacterium that causes the bubonic plague—experienced a genetic tweak that allowed rodents to live longer after they were infected, according to a new study. This alteration may have prolonged two significant plague pandemics, including the deadliest event in human history: the Black Death. Researchers at the Institut Pasteur in France and McMaster University in Canada studied hundreds of ancient Y. pestis DNA samples to investigate a gene called 'pla.' Their study, published May 29 in the journal Science, identified a decrease in repetitions of the pla gene in the Y. pestis genome during the later stages of both the first and second major plague pandemics. The researchers believe these pla depletions ultimately allowed these pandemics to last longer. The first plague pandemic, known as the Plague of Justinian, struck the Mediterranean basin during the sixth century and caused tens of millions of deaths over the course of two centuries. The second emerged when the Black Death broke out in 1347, killing an estimated 30% to 50% of Europe's population in just six years. But this was just the beginning. Like the first pandemic, this plague continued to reemerge for centuries, lasting more than 500 years. This newly discovered evolution of the pla gene offers more insight into how these plagues persisted for so long. The pla gene appears many times in the Y. pestis' genome and plays a crucial role in its virulence by allowing it to infect the lymph nodes before traveling to the rest of the body, according to an Institut Pasteur statement. This causes rapid septicemia—or blood poisoning—and quickly kills the victim. Therefore, a lack of this gene in Y. pestis strains from the first and second major pandemics likely made the bacterium less virulent, the researchers suggest. To test that hypothesis, they infected mice with three preserved strains of Y. pestis from the third major pandemic that also had fewer repetitions of pla. 'These three samples enabled us to analyze the biological impact of these pla gene deletions,' said co-author Javier Pizarro-Cerdá, director of the Yersinia Research Unit at the Institut Pasteur, according to the statement. Through their mouse model, Pizarro-Cerdá and his colleagues found that the pla depletion resulted in a 20% decrease in victim mortality. What's more, it allowed infected rodents to live significantly longer. Based on these findings, the researchers concluded that rats infected with pla-depleted Y. pestis strains may have been more effective disease vectors, as they had more time to spread the plague far and wide before they died. Rodents—particularly rats—played a critical role in spreading the bubonic plague to humans. People most commonly contract this disease via infected flea bites, and fleas typically contract it when they feed on infected rodents. Thus, an increase in the lifespans of sickened rodents would have provided greater opportunity for fleas to bite them, become infected, and then bite humans. 'Ours is one of the first research studies to directly examine changes in an ancient pathogen, one we still see today, in an attempt to understand what drives the virulence, persistence, and eventual extinction of pandemics,' said co-lead author Hendrik Poinar, director of the McMaster Ancient DNA Centre and holder of the Michael G. DeGroote Chair in Genetic Anthropology, according to the statement. Today, the bubonic plague is considered a rare disease, though a small number of cases still emerge in western North America, Africa, Asia, and South America, according to the Cleveland Clinic. While this research provides valuable insight into the evolutionary history of Y. pestis and the world-altering pandemics it caused, it can also serve as a model for better understanding how deadly diseases emerge and spread, according to the researchers.
Fox News
05-06-2025
- Health
- Fox News
New study reveals leprosy existed in the Americas before European explorers arrived
Scientists say a species of bacteria rewrites the history of when an infectious and potentially deadly disease first arrived in the Americas. And it was long before the arrival of European explorers. Researchers from the Institut Pasteur in Paris, France, with help from a U.S. university, recently announced in a news release that a second species of bacteria is also responsible for the disease known as leprosy, or Hansen's disease, in the Americas. In years past, many believed that the bacterium known as Mycobacterium leprae caused leprosy and that it was only spread in America by early European explorers and settlers. However, the revelation of a second bacterium puts that theory of blaming the settlers on its head, as an existing strain was already on the continents calling the New World home. The bacterium Mycobacterium lepromatosis existed and infected humans for 1,000 years prior to Europeans arriving, researchers say. Dr. Maria Lopopolo, the first author of the study and researcher at the Laboratory of Microbial Paleogenomics at the Institut Pasteur, said it changes everything about leprosy in the Americas. "This discovery transforms our understanding of the history of leprosy in America. It shows that a form of the disease was already endemic among Indigenous populations well before the Europeans arrived," she said in the release. The study — led by scientists from the Laboratory of Microbial Paleogenomics at the Institut Pasteur, alongside the French National Center for Scientific Research, and the University of Colorado in the U.S. — began after Mycobacterium lepromatosis was found in a Mexican patient in 2008, and red squirrels in the British Isles in 2016. Using advanced genetic techniques to reconstruct the genomes of Mycobacterium lepromatosis from ancient individuals from Argentina and Canada, scientists found that the two strains from the different regions were genetically close in the Mycobacterium genome family tree, meaning that the bacteria spread rapidly throughout the continent. The release stated that the results confirmed that Mycobacterium lepromatosis had already spread throughout North and South America. Researchers worked in collaboration with indigenous communities, various international institutions and archaeologists, according to the release, and were able to study over 800 DNA samples from ancient human remains and recent medical cases showing signs of leprosy. Nicolás Rascovan, the lead author of the study at the Institut Pasteur, said that the research proves that human history can be changed. "We are just beginning to uncover the diversity and global movements of this recently identified pathogen," he said. "This study allows us to hypothesize that there might be unknown animal reservoirs." The Centers for Disease Control and Prevention (CDC) says leprosy can affect the nerves, skin and eyes of patients, and is treated with antibiotics. Up to 225 people in the U.S., and 250,000 around the world, contract Hansen's disease, according to the CDC.
