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Two Studies Find Gut Fungi Drive Childhood Allergy Risk, With Mouse Research Pointing to Infant Antibiotics as a Culprit

In A Nutshell

  • Two studies published together in Nature Communications found that gut fungi, particularly a yeast called Malassezia, play a previously overlooked role in early-life immune development and allergic disease risk.
  • A large Canadian cohort study of more than 1,400 infants found that babies with delayed fungal gut development were more likely to develop atopic dermatitis and food allergy by age five.
  • A separate study found that infant antibiotic use triggered a surge of Malassezia in the gut, and mouse experiments showed that yeast drove immune changes and worsened asthma-like airway inflammation.
  • Together, the studies position the gut’s fungal community as a promising new target for preventing childhood allergic diseases.

Hundreds of millions of children worldwide live with allergic diseases, and the number keeps climbing. Scientists have spent decades studying the bacterial side of the gut microbiome for clues about why, but two studies published together in Nature Communications point toward a part of that ecosystem that has been almost entirely overlooked: the fungi.

Conducted by separate teams at the University of Calgary and BC Children’s Hospital, both studies converged on the same yeast, called Malassezia, from two very different directions. One team tracked gut fungal development in more than 1,400 Canadian infants and found that babies whose fungal communities matured slowly were more likely to develop atopic dermatitis and food allergy by age five. The other found that infant antibiotics triggered a surge of that same yeast and showed, in mouse models, that it drove immune changes tied to asthma-like airway inflammation. Neither team knew the other had been working on the same fungus until they compared notes.

“Hundreds of millions of children worldwide are affected by allergic diseases, and the number is growing,” said Dr. Stuart Turvey, senior author of the cohort study and a professor of pediatrics at the University of British Columbia. “A better understanding of what gives rise to these conditions and how we can prevent them would have an enormous benefit for children around the globe.”

A Gut Fungus That Tracks With Allergic Disease Risk

Turvey’s team analyzed stool samples from 1,409 participants in the CHILD Cohort Study, a large Canadian birth cohort that follows children from pregnancy through early childhood. By generating fungal sequencing data from 2,256 samples collected at around three months and one year of age, the researchers were able to map how the gut’s fungal community changes during the first year of life.

One pattern stood out immediately. Malassezia was abundant early on and then declined sharply over the first year, while a group of yeasts called Saccharomycetaceae followed the opposite trajectory, increasing steadily with age. Babies whose fungal communities hadn’t followed that expected developmental arc at twelve months, showing a pattern more typical of younger infants, were significantly more likely to be diagnosed with atopic dermatitis or food allergy by the time they turned five. Malassezia was the single strongest fungal predictor of where a baby’s gut microbiome stood developmentally.

gut fungi infographic
Two studies find gut fungi, especially Malassezia, may drive childhood asthma and allergies, and infant antibiotics could be fueling the problem. (Image by StudyFinds)

Antibiotics, Fungi, and the Immune System

Led by Dr. Marie-Claire Arrieta at the University of Calgary, a second team approached the same fungus from a different angle. Working with 47 infants under six months old who came to Alberta Children’s Hospital’s emergency department needing injectable antibiotics, researchers collected stool samples before and after treatment to analyze bacterial and fungal gut communities.

Antibiotics knocked back bacterial diversity, as expected, but had the opposite effect on fungi. Fungal diversity increased in roughly 79% of the short-term treatment group. One genus expanded more than any other: Malassezia. The single factor most strongly associated with that expansion, even after accounting for birth weight and gestational age, was the total number of different antibiotics a baby received.

To test what that surge could mean for a developing immune system, the team raised mice under sterile conditions and introduced a controlled bacterial community with or without M. restricta, the Malassezia species that had expanded most in the infants. At just three weeks old, the fungus-colonized mice showed a markedly different immune profile, with higher numbers of cells tied to allergic disease and asthma risk, changes that extended beyond the gut into the lymph nodes. When those mice were later exposed to house dust mite, a common asthma trigger, they developed significantly worse airway inflammation. Mice that also had an early RSV infection showed even greater susceptibility to allergic airway inflammation later in life.

“Antibiotics are an essential treatment for young children when needed, but this study shows that there is a previously overlooked effect on the gut mycobiome, allowing species like Malassezia to flourish, and directly impacting immunological function,” said Dr. Arrieta.

A New Frontier for Treating Childhood Allergies

Taken together, the studies make a case that the fungal side of the gut has been a costly blind spot. Bacterial disruption has dominated the conversation around early-life microbiome research for years. These two papers, arriving from independent teams using entirely different methods, both land on the same fungus and the same conclusion: Malassezia is not a passive inhabitant of the infant gut. At critical windows of development, it may actively shape how a child’s immune system learns to respond to the world. Whether that knowledge can one day be used to prevent allergic diseases remains to be seen, but researchers now have a clear target to aim at.


Disclaimer: This article is based on two peer-reviewed studies. The mouse findings are promising but have not been confirmed in human clinical trials. The infant antibiotic study was observational and did not include an untreated control group. Readers should not alter any medical decisions for themselves or their children based on this research alone. Always consult a qualified healthcare provider with any questions about infant health, allergies, or asthma risk.


Paper Notes

Limitations

The ANTIBIO clinical study enrolled 47 infants but did not include an age-matched untreated control group. Because detailed clinical diagnoses for why each infant received antibiotics were not available, researchers could not rule out whether the underlying illness, rather than antibiotics alone, contributed to the observed fungal changes. The cohort was not large enough to determine whether specific antibiotic classes had different effects on fungal communities. The mouse models used a simplified bacterial community that cannot fully replicate the complexity of a real infant gut. The CHILD Cohort Study, while large, is subject to confounding variables common to longitudinal observational designs, and the fungal maturation findings are associative rather than causal. Neither study was designed to determine whether Malassezia expansion was temporary or whether it directly caused later allergic diagnoses.

Funding and Disclosures

The Arrieta lab study was supported by funding to senior author Marie-Claire Arrieta from the Cumming School of Medicine, the Alberta Children’s Hospital Research Institute, the Snyder Institute for Chronic Diseases, CIHR Project Grant 180429, the SickKids Foundation, the Weston Family Microbiome Grant, and BREATHE, The Lung Association of Canada. Lead author Erik van Tilburg Bernardes was funded by the Eyes High Doctoral Recruitment Scholarship and a CIHR doctoral award. The CHILD Cohort Study received core support from the Canadian Institutes of Health Research and the AllerGen Network of Centres of Excellence. Senior author Stuart Turvey holds a Tier 1 Canada Research Chair in Pediatric Precision Health. The authors of both studies declare no competing interests.

Publication Details

Study 1 Authors: Erik van Tilburg Bernardes, Thaís Glatthardt, Mackenzie W. Gutierrez, William N.T. Nguyen, Emily M. Mercer, Hena R. Ramay, Carolyn A. Thomson, Tisha Belle A. Halim, Nithya Gopalakrishnan, Katarina MacConnell, Kristen Kalbfleisch, Kamala D. Patel, Eugenia Corrales-Aguilar, Kathy D. McCoy, Stephen B. Freedman, and Marie-Claire Arrieta | Study 1 Title: “Antibiotic-induced Malassezia expansion in the infant gut promotes early-life immune dysregulation and airway inflammation in mice” | DOI: 10.1038/s41467-026-74417-x | Study 2 Authors: Courtney Hoskinson, Darlene L.Y. Dai, Charisse Petersen, Theo J. Moraes, Piushkumar J. Mandhane, Elinor Simons, Anita L. Kozyrskyj, Meghan B. Azad, Padmaja Subbarao, and Stuart E. Turvey | Study 2 Title: “Saccharomycetes and Malassezia fungi associate with early-life gut maturation and allergic disease risk in childhood” | DOI: 10.1038/s41467-026-74418-w | Journal: Nature Communications (2026)

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