The human gut microbiome shapes vaccine side effects
Summary author: Walter Beckwith
A person’s microbiome may help determine whether they develop a fever after receiving a vaccination, according to a new study. The findings suggest that the microbiome and potentially diet could one day be targeted to reduce vaccine-related inflammation without compromising the immune protection vaccines provide. Vaccines are a crucial tool for ensuring public health, but people vary widely in their immune responses and side effects. Fever and flu-like symptoms are among the most common adverse reactions to vaccines, particularly mRNA- and lipid nanoparticle-based vaccines. These reactions can discourage future vaccination and contribute to vaccine hesitancy and mistrust. However, not all those who receive a vaccination develop a fever and those who do tend to get a fever across repeated doses, suggesting the importance of individual risk factors for fever. The reasons for this variation are not well understood.
In this study, Kelsey Huus and colleagues speculated that the gut microbiome, which is known to influence immune activity, may play a role in driving these reactions. To test this hypothesis, Huus et al. profiled the fecal microbiomes, body temperature, and blood-based immune markers of 171 healthy adults before and after receiving the mRNA vaccination for SARS-CoV-2. The findings showed that certain gut bacteria, especially Lachnospiraceae, produce flagellin, which can activate inflammatory immune pathways and intensify vaccine-related reactions. Those who had greater pre-vaccination intestinal inflammation or higher levels of flagellin expression in the gut tended to develop vaccine-induced fever. What’s more, the authors found that industrialized diets may promote this inflammatory activity. Vegetarian diets tended to correlate with microbiome features that contributed to less fever, while lower consumption of whole plant foods and diets characterized by greater fat or processed-food intake were associated with the inflammatory, fever-associated microbiome. Dietary manipulation altered both microbiome compositions and their associated vaccine responses. Importantly, Huus et al. show that flagellin, inflammation, and diet do not affect antibody responses to vaccines, suggesting that the microbiome-driven inflammation increased vaccine side effects without necessarily affecting immunity. “Diet, microbial ecology, and the metabolic state are not immutable, and people might one day prepare for vaccination as deliberately as the vaccine itself is formulated,” writes Bali Pulendran in a related Perspective.
Journal
Science
Article Title
The human gut microbiome primes fever after vaccination
Article Publication Date
8-Oct-2026
Chronic intestinal inflammation can affect heart through changes in gut microbiota and immune cells, study finds
Georgia State University
image:
Jun Zou, an assistant professor in the Institute for Biomedical Sciences at Georgia State University
view moreCredit: Georgia State University
ATLANTA — Chronic intestinal inflammation drives cardiac dysfunction through a gut microbiota-dependent mediated pathway, suggesting a potential therapeutic target for reducing cardiovascular risk in patients with inflammatory bowel disease (IBD), according to a study led by researchers in the Institute for Biomedical Sciences at Georgia State University.
The findings published in Circulation Research demonstrated that chronic colitis (inflammation of the colon)-associated gut microbiota dysbiosis (an imbalance in the different microorganisms living together in a microbiome) causally contributes to cardiac hypertrophy and cardiac dysfunction by driving systemic immune cell metabolic and mitochondrial reprogramming in mice. Mitochondria are cell organelles that generate most of the chemical energy needed to power the cell’s biochemical reactions.
Cardiovascular disease is a leading cause of global morbidity and mortality. People with IBD, which includes chronic inflammatory conditions of the digestive tract, have an increased risk of cardiovascular complications. IBD is also associated with changes in the gut microbiota, the community of microorganisms that normally lives in the intestine. However, exactly how these changes in the gut contribute to heart problems has remained unclear.
In this study, the researchers used a chronic colitis mouse model to assess gut microbiota dysbiosis, systemic immune cell metabolism and cardiac remodeling. Transferring gut microbiota from mice with colitis to healthy mice was sufficient to alter immune cell metabolism and promote cardiac abnormalities, providing evidence that changes in gut microbes can contribute to the effects of intestinal inflammation on the heart.
Furthermore, the researchers identified a bacterial component called lipopolysaccharide, or LPS, as an important link between the gut and heart. LPS is produced by certain types of gut bacteria and can enter the circulation when the intestinal environment is disrupted. The study found that increased LPS stimulates immune cells to produce a protein called GBP1, leading to changes in these cells that promote their recruitment to the heart.
“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.”
The study also revealed another way GBP1 may affect the heart. During colitis, GBP1 was increased in exosomes, tiny packages released by cells that circulate in the body and carry biological signals between cells. The researchers found that these GBP1-containing exosomes could be taken up by heart cells and contribute to their enlargement.
“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 associate 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.”
The study was funded by the National Heart, Lung, and Blood Institute of the National Institutes of Health.
Additional authors of the study include Yadong Wang, Jian Li, Junqing An, Vu L. Ngo, Shuhan Wang, Zhenkai Hao, Chao Li and Hirohito Abo of the Institute for Biomedical Sciences at Georgia State.
To read the study, visit https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.126.329058.
Journal
Circulation Research
Method of Research
Experimental study
Subject of Research
Animals
Article Title
Gut Dysbiosis Promotes Myocardial Hypertrophy via GBP2b/GBP1 in Chronic Colitis
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