Latest news with #OsakaUniversity
Yahoo
7 days ago
- Health
- Yahoo
Researchers find a link between gut bacteria and genes in colitis flare-ups
Researchers have identified a gut-genetic interaction that could trigger an overactive immune response in the colon — offering one possible explanation for the pain and bleeding of ulcerative colitis, and why it behaves so differently from patient to patient. Their research is published Friday in the journal Science Immunology. Ulcerative colitis is a chronic disease that affects more than 1.2 million people in the United States, according to a 2023 study of medical claims data. It falls under the umbrella of inflammatory bowel disease, or IBD — a group of conditions that includes Chron's disease and is marked by unpredictable flare-ups, long-term discomfort, and treatments that often work inconsistently. 'This study demonstrates that it's not just an imbalance of microbes in your gut or genetics that induce intestinal inflammation — but the interaction between the two,' said Hisako Kayama, an associate professor of immunology at Osaka University and co-senior author of the study. At the center of that inflammatory response is a protein called STING that helps the body recognize the DNA of bacteria and viruses and mount an immune response. Healthy people are able to keep this response under control with the help of a gene called OTUD3, which acts as a biological brake. But in some people, their OTUD3 gene variant leads that brake to fail — causing the immune system to treat harmless bacteria as a threat. Unchecked, the protein can drive chronic inflammation, particularly in the gut, which is home to many different types of "good" bacteria. The protein STING is very important in fighting bacterial infections, said co-author Dr. Kiyoshi Takeda, a professor of immunology at Osaka University. 'But the problem is that the overactivation of STING causes inflammation.' To explore how this interaction plays out, the researchers studied mice bred specially to have a genetic vulnerability to colitis similar to humans. When feces from the ulcerative colitis patients was transferred to the colons of the mice, they developed more severe colitis symptoms than mice with a normal version of the gene. If they didn't have the gene variant or the microbial trigger, the disease didn't develop. In total, researchers used tissue and gut bacteria from 124 patients — including 65 with ulcerative colitis and 59 with colorectal cancer — plus 12 healthy people as controls. The culprit was a molecule called cGAMP, which is made by certain gut bacteria. In healthy mice, researchers know that OTUD3 helps break down excess cGAMP so the immune system doesn't overreact. But in mice without a working version of that gene, cGAMP built up, overactivating STING and causing inflammation. The findings could help explain why some patients respond poorly to current ulcerative colitis treatments, which typically suppress the immune system as a whole. By pinpointing a single inflammatory pathway, the study opens the door to more precise, personalized therapies — especially for patients who carry this specific gene variant. Still, the researchers caution that any treatment targeting the STING protein directly must be used carefully, since suppressing it too much could leave patients vulnerable to infection. Alternative approaches, such as targeting cGAMP-producing bacteria, could allow STING to keep doing its job in the rest of the body while dialing down inflammation in the colon. The variant gene that colitis sufferers have is common. According to past genome-wide studies, it appears in about 53% of Europeans, 52% of Americans and 16% of Japanese people. Not everyone with it develops the disease, lending credence to the idea that it's the interaction between genes and microbes that triggers inflammation. 'This study is helpful in demonstrating a specific example — a genetic variant and a microbial signal — that leads to inflammation,' said Dr. Jonathan Jacobs, a gastroenterologist and microbiome researcher at UCLA who was not involved with the study. 'That's exciting," he said, because it offers a clear mechanism that ties together many of the risk factors scientists have long observed in inflammatory bowel disease. Even if it turns out not many people are vulnerable to this particular gut-genetic interaction, he said, the research could lead to more personalized treatment. 'It moves us closer to precision medicine,' Jacobs said. The shift toward more targeted treatment could make a world of difference for patients like Anderson Hopley, a volunteer with the Orange County and Los Angeles chapter of the Crohn's and Colitis Foundation who was diagnosed with Crohn's this year. 'I know people who have medication that'll work for a couple years, maybe even just a couple months, and then it kind of randomly stops,' he said. 'They have to adjust everything.' Although Hopley has Crohn's, not ulcerative colitis, he said the new study still resonates. 'I think it'd be really nice to know what causes this,' he said. 'Even if there's not a cure yet, just having an answer — some clarity — would be a step in the right direction.' This story originally appeared in Los Angeles Times. Solve the daily Crossword
Los Angeles Times
7 days ago
- Health
- Los Angeles Times
Researchers find a link between gut bacteria and genes in colitis flare-ups
LOS ANGELES — Researchers have identified a gut-genetic interaction that could trigger an overactive immune response in the colon — offering one possible explanation for the pain and bleeding of ulcerative colitis, and why it behaves so differently from patient to patient. Their research is published Friday in the journal Science Immunology. Ulcerative colitis is a chronic disease that affects more than 1.2 million people in the United States, according to a 2023 study of medical claims data. It falls under the umbrella of inflammatory bowel disease, or IBD — a group of conditions that includes Chron's disease and is marked by unpredictable flare-ups, long-term discomfort, and treatments that often work inconsistently. 'This study demonstrates that it's not just an imbalance of microbes in your gut or genetics that induce intestinal inflammation — but the interaction between the two,' said Hisako Kayama, an associate professor of immunology at Osaka University and co-senior author of the study. At the center of that inflammatory response is a protein called STING that helps the body recognize the DNA of bacteria and viruses and mount an immune response. Healthy people are able to keep this response under control with the help of a gene called OTUD3, which acts as a biological brake. But in some people, their OTUD3 gene variant leads that brake to fail — causing the immune system to treat harmless bacteria as a threat. Unchecked, the protein can drive chronic inflammation, particularly in the gut, which is home to many different types of 'good' bacteria. The protein STING is very important in fighting bacterial infections, said co-author Dr. Kiyoshi Takeda, a professor of immunology at Osaka University. 'But the problem is that the overactivation of STING causes inflammation.' To explore how this interaction plays out, the researchers studied mice bred specially to have a genetic vulnerability to colitis similar to humans. When feces from the ulcerative colitis patients was transferred to the colons of the mice, they developed more severe colitis symptoms than mice with a normal version of the gene. If they didn't have the gene variant or the microbial trigger, the disease didn't develop. In total, researchers used tissue and gut bacteria from 124 patients — including 65 with ulcerative colitis and 59 with colorectal cancer — plus 12 healthy people as controls. The culprit was a molecule called cGAMP, which is made by certain gut bacteria. In healthy mice, researchers know that OTUD3 helps break down excess cGAMP so the immune system doesn't overreact. But in mice without a working version of that gene, cGAMP built up, overactivating STING and causing inflammation. The findings could help explain why some patients respond poorly to current ulcerative colitis treatments, which typically suppress the immune system as a whole. By pinpointing a single inflammatory pathway, the study opens the door to more precise, personalized therapies — especially for patients who carry this specific gene variant. Still, the researchers caution that any treatment targeting the STING protein directly must be used carefully, since suppressing it too much could leave patients vulnerable to infection. Alternative approaches, such as targeting cGAMP-producing bacteria, could allow STING to keep doing its job in the rest of the body while dialing down inflammation in the colon. The variant gene that colitis sufferers have is common. According to past genome-wide studies, it appears in about 53% of Europeans, 52% of Americans and 16% of Japanese people. Not everyone with it develops the disease, lending credence to the idea that it's the interaction between genes and microbes that triggers inflammation. 'This study is helpful in demonstrating a specific example — a genetic variant and a microbial signal — that leads to inflammation,' said Dr. Jonathan Jacobs, a gastroenterologist and microbiome researcher at UCLA who was not involved with the study. 'That's exciting,' he said, because it offers a clear mechanism that ties together many of the risk factors scientists have long observed in inflammatory bowel disease. Even if it turns out not many people are vulnerable to this particular gut-genetic interaction, he said, the research could lead to more personalized treatment. 'It moves us closer to precision medicine,' Jacobs said. The shift toward more targeted treatment could make a world of difference for patients like Anderson Hopley, a volunteer with the Orange County and Los Angeles chapter of the Crohn's and Colitis Foundation who was diagnosed with Crohn's this year. 'I know people who have medication that'll work for a couple years, maybe even just a couple months, and then it kind of randomly stops,' he said. 'They have to adjust everything.' Although Hopley has Crohn's, not ulcerative colitis, he said the new study still resonates. 'I think it'd be really nice to know what causes this,' he said. 'Even if there's not a cure yet, just having an answer — some clarity — would be a step in the right direction.'
Japan Times
11-07-2025
- Science
- Japan Times
Mouse embryo implantation reproduced in lab equipment
A team led by a professor at Osaka University's Bioinformatics Center has replicated the mouse embryo implantation process in laboratory equipment with a high success rate. Masahito Ikawa and his team on Wednesday said that they had developed a method of culturing fragments of uterine tissue from mice in laboratory containers to achieve embryo implantation. The team also discovered protein interactions that help drive embryo implantation.
10-07-2025
- Health
Mouse Embryo Implantation Reproduced in Lab Equipment
News from Japan Society Jul 10, 2025 20:10 (JST) Osaka, July 10 (Jiji Press)--A team led by a professor at Osaka University's Bioinformatics Center has replicated the mouse embryo implantation process in laboratory equipment with a high success rate. Masahito Ikawa and his team on Wednesday said that they have developed a method of culturing fragments of uterine tissue from mice in laboratory containers to achieve embryo implantation. The team also discovered an interplay in a protein necessary for implantation. Its findings were published in the British scientific journal Nature Communications. "We hope to develop a method to improve implantation failure as much as possible in assisted reproductive technology for humans and a therapeutic drug" through the developed technique, Ikawa said. [Copyright The Jiji Press, Ltd.] Jiji Press
News18
07-07-2025
- Health
- News18
Birth Without Pregnancy: Lab Eggs And Sperm Closer To Reality Than You Think
Last Updated: In-vitro gametogenesis (IVG) could allow humans to create eggs and sperm from skin or blood cells within 5 to 7 years, revolutionising reproduction and challenging norms What was once the stuff of futuristic fantasy is now on the verge of becoming a reality. Scientists around the world are racing to develop in-vitro gametogenesis (IVG) — a revolutionary technology that could allow humans to create eggs and sperm from skin or blood cells, potentially enabling childbirth without traditional pregnancy. At the forefront of this scientific frontier is Professor Katsuhiko Hayashi of Osaka University, Japan, whose lab is pushing the boundaries of what we know about human reproduction. The Promise Of IVG: A New Era Of Parenthood In an interview with The Guardian, Professor Hayashi revealed that his lab could produce fully functional human eggs and sperm in just seven years. This means a future where: A woman gives birth without ever being pregnant Two men become biological fathers A person creates a child using only their own DNA While this may sound like science fiction, it's fast becoming a scientific possibility. Global Race To Revolutionise Fertility Japan isn't the only country investing in this bold future. In the United States, Conception Biosciences, a Silicon Valley startup led by Matt Krisiloff, claims their lab-based fertility solutions could reach clinics in as little as five years. Armed with significant funding, their aim is not just to treat infertility but to reshape the very idea of family and reproduction. In a landmark mouse experiment, researchers successfully created a female mouse using the sperm of two males, a proof-of-concept that's now being translated to human biology. IVG begins with stem cells derived from human skin or blood. In Professor Hayashi's lab, scientists have created tiny testicular and ovarian organoids — 1 mm sized structures that mimic real reproductive organs. These lab-grown organs are already producing precursor sex cells, though challenges remain in sustaining their growth. Current hurdles include ensuring oxygen supply, cell stability, and avoiding genetic defects. Another breakthrough includes the development of ovary organoids, which are now capable of progressing toward full human egg development. What The Future Holds: Hopes And Controversies If successful, IVG could radically alter options for people struggling with infertility or those traditionally excluded from biological parenthood. It opens the door for: But with innovation comes uncertainty. IVG raises serious ethical, legal, and religious questions. Issues of genetic health, societal acceptance, and long-term effects remain largely unanswered. Global Status And Ethical Landscape Currently, IVG is banned in the UK, though the US and Japan continue to fund and accelerate research. Professor Saito of Kyoto University and several American startups, including Conception Biosciences, are actively competing in this rapidly evolving space. While the timeline is uncertain, experts believe that within a decade, the first child born from lab-made eggs or sperm could become a reality, marking a profound shift in how we understand human life. First Published: July 07, 2025, 12:25 IST
