{"id":73953,"date":"2025-07-18T23:55:09","date_gmt":"2025-07-18T23:55:09","guid":{"rendered":"https:\/\/www.europesays.com\/us\/73953\/"},"modified":"2025-07-18T23:55:09","modified_gmt":"2025-07-18T23:55:09","slug":"a-link-between-gut-bacteria-and-genes-in-colitis-flare-ups","status":"publish","type":"post","link":"https:\/\/www.europesays.com\/us\/73953\/","title":{"rendered":"A link between gut bacteria and genes in colitis flare-ups"},"content":{"rendered":"\n

LOS ANGELES\u00a0\u2014\u00a0Researchers have identified a gut-genetic interaction that could trigger an overactive immune response in the colon \u2014 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<\/a>.<\/p>\n

Ulcerative colitis is a chronic disease that affects more than 1.2 million people in the United States<\/a>, according to a 2023 study of medical claims data. It falls under the umbrella of inflammatory bowel disease, or IBD \u2014 a group of conditions that includes Chron\u2019s disease and is marked by unpredictable flare-ups, long-term discomfort, and treatments that often work inconsistently.<\/p>\n

\u201cThis study demonstrates that it\u2019s not just an imbalance of microbes in your gut or genetics that induce intestinal inflammation \u2014 but the interaction between the two,\u201d said Hisako Kayama, an associate professor of immunology at Osaka University and co-senior author of the study.<\/p>\n

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 \u2014 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 \u201cgood\u201d bacteria<\/a>. <\/p>\n

The protein STING is very important in fighting bacterial infections, said co-author Dr. Kiyoshi Takeda, a professor of immunology at Osaka University. \u201cBut the problem is that the overactivation of STING causes inflammation.\u201d<\/p>\n

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\u2019t have the gene variant or the microbial trigger, the disease didn\u2019t develop.<\/p>\n

In total, researchers used tissue and gut bacteria from 124 patients \u2014 including 65 with ulcerative colitis and 59 with colorectal cancer \u2014 plus 12 healthy people as controls. <\/p>\n

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\u2019t overreact. But in mice without a working version of that gene, cGAMP built up, overactivating STING and causing inflammation. <\/p>\n

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 \u2014 especially for patients who carry this specific gene variant.<\/p>\n

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.<\/p>\n

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\u2019s the interaction between genes and microbes that triggers inflammation.<\/p>\n

\u201cThis study is helpful in demonstrating a specific example \u2014 a genetic variant and a microbial signal \u2014 that leads to inflammation,\u201d said Dr. Jonathan Jacobs, a gastroenterologist and microbiome researcher at UCLA who was not involved with the study. \u201cThat\u2019s exciting,\u201d he said, because it offers a clear mechanism that ties together many of the risk factors scientists have long observed in inflammatory bowel disease. <\/p>\n

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. \u201cIt moves us closer to precision medicine,\u201d Jacobs said.<\/p>\n

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\u2019s and Colitis Foundation who was diagnosed with Crohn\u2019s this year.<\/p>\n

\u201cI know people who have medication that\u2019ll work for a couple years, maybe even just a couple months, and then it kind of randomly stops,\u201d he said. \u201cThey have to adjust everything.\u201d<\/p>\n

Although Hopley has Crohn\u2019s, not ulcerative colitis, he said the new study still resonates. <\/p>\n

\u201cI think it\u2019d be really nice to know what causes this,\u201d he said. \u201cEven if there\u2019s not a cure yet, just having an answer \u2014 some clarity \u2014 would be a step in the right direction.\u201d<\/p>\n","protected":false},"excerpt":{"rendered":"LOS ANGELES\u00a0\u2014\u00a0Researchers have identified a gut-genetic interaction that could trigger an overactive immune response in the colon \u2014…\n","protected":false},"author":3,"featured_media":73954,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[26],"tags":[11399,51630,51634,15094,815,33982,51635,48523,51633,13987,3546,1929,26298,159,51632,7572,51631,67,132,68],"class_list":{"0":"post-73953","1":"post","2":"type-post","3":"status-publish","4":"format-standard","5":"has-post-thumbnail","7":"category-genetics","8":"tag-chronic-disease","9":"tag-chronic-inflammation","10":"tag-colitis-flare-up","11":"tag-gene","12":"tag-genetics","13":"tag-gut-bacteria","14":"tag-interaction","15":"tag-mouse","16":"tag-otud3-gene-variant","17":"tag-patient","18":"tag-people","19":"tag-protein","20":"tag-researcher","21":"tag-science","22":"tag-sting","23":"tag-study","24":"tag-ulcerative-colitis","25":"tag-united-states","26":"tag-unitedstates","27":"tag-us"},"share_on_mastodon":{"url":"https:\/\/pubeurope.com\/@us\/114876941927941974","error":""},"_links":{"self":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts\/73953","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/users\/3"}],"replies":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/comments?post=73953"}],"version-history":[{"count":0,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts\/73953\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/media\/73954"}],"wp:attachment":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/media?parent=73953"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/categories?post=73953"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/tags?post=73953"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}