Plate Nº 98 · recorded October 9, 2026
Health & Medicine ResearchReported finding
Gut Inflammation Can Damage the Heart — Through Microbes and Immune Cells
Georgia State researchers show in mice that gut microbes from colitic animals alone can trigger immune changes that enlarge and weaken the heart, via a bacterial molecule called LPS.
By James Calloway3 min read673 words
In brief
- The study was published in Circulation Research in 2026 (DOI: 10.1161/circresaha.126.329058).
- Transferring gut microbiota from mice with colitis to healthy mice was sufficient to promote cardiac abnormalities.
- The identified pathway runs from bacterial LPS to immune-cell production of the protein GBP1.
- GBP1 travels both in immune cells recruited to the heart and in exosomes taken up by heart cells.
Chronic intestinal inflammation can drive heart dysfunction by reshaping gut microbes and reprogramming immune cells, according to a study led by researchers at Georgia State University's Institute for Biomedical Sciences and published in the journal Circulation Research in 2026.
Working in mice, the team showed that the microbial imbalance linked to chronic colitis — inflammation of the colon — causally contributes to cardiac hypertrophy (an abnormal enlargement of the heart muscle) and impaired heart function. The mechanism involves metabolic and mitochondrial reprogramming of immune cells throughout the body. Mitochondria are the tiny structures inside cells that produce most of the chemical energy a cell needs.
The findings matter because people with inflammatory bowel disease (IBD), a group of chronic inflammatory conditions of the digestive tract, face a heightened risk of cardiovascular complications. Cardiovascular disease remains a leading cause of illness and death worldwide. Scientists have known that IBD alters the gut microbiota — the community of microorganisms normally living in the intestine — but exactly how those changes translate into heart problems has been unclear.
What did the experiments show?
The researchers used a mouse model of chronic colitis to examine three things at once: gut microbiota dysbiosis (an imbalance among the microorganisms living in a microbiome), the metabolism of systemic immune cells, and cardiac remodeling — structural changes in the heart.
The most decisive experiment involved fecal transfer. When the researchers transplanted gut microbiota from mice with colitis into healthy mice, the recipients developed altered immune cell metabolism and cardiac abnormalities. Nothing else was needed. This provides direct evidence that changes in gut microbes alone can contribute to the effects of intestinal inflammation on the heart.
How do bacterial signals reach the heart?
The study identifies a specific molecular culprit: lipopolysaccharide, or LPS. LPS is a component of certain gut bacteria. When the intestinal environment is disrupted, it can leak into the bloodstream.
Once in circulation, increased levels of LPS stimulate immune cells to produce a protein called GBP1. That protein changes the immune cells in ways that promote their recruitment — their movement and accumulation — in the heart. There, the cells can contribute to abnormal heart enlargement and impaired function.
"Our study provides evidence that chronic intestinal inflammation can affect the heart through changes in the gut microbiota and immune cells," said Jun Zou, an assistant professor in the Institute for Biomedical Sciences at Georgia State. "We found that bacterial signals from the gut can alter immune cells in ways that promote their movement into the heart, where they can contribute to abnormal heart enlargement and impaired function."
Is there a second route of damage?
Yes. The researchers found that GBP1 can reach the heart by an additional path. During colitis, GBP1 levels rose in exosomes — tiny packages that cells release, which circulate in the body and carry biological signals between cells.
Heart cells can take up these GBP1-containing exosomes directly. Once inside, the protein contributes to the enlargement of those heart cells, adding a second mechanism by which gut-driven inflammation stresses the heart.
What are the broader implications?
The results point toward a potential therapeutic target for reducing cardiovascular risk in patients with IBD. If excessive GBP1 activation helps drive cardiac dysfunction, dampening that pathway could protect the heart — though any clinical application remains speculative for now, as the findings come from mouse models and have not yet been demonstrated in humans.
The work may also extend beyond IBD. "This work may also have broader implications for infection-associated cardiac injury, as many pathogens strongly induce GBP family proteins," said Ye Ding, co-senior author of the study and a research assistant professor in the Institute for Biomedical Sciences at Georgia State. "While GBP1 plays essential antimicrobial roles during infection, excessive or dysregulated GBP1 activation may inadvertently contribute to cardiac dysfunction."
In other words, a protein that normally helps the body fight microbes may, when overactivated, become part of a pathway that harms the heart.
The study, by Yadong Wang and colleagues, appears in Circulation Research (2026), DOI: 10.1161/circresaha.126.329058.
via Medical Xpress (Source)
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