Gut microbes from healthy infants block milk allergy development in mice

NIH-funded study links gut microbiome to food allergy

IMAGE

Credit: The University of Chicago


WHAT:

New research suggests that the gut microbiome may help prevent the development of cow’s milk allergy. Scientists at the University of Chicago found that gut microbes from healthy human infant donors transplanted into mice protected animals exposed to milk from experiencing allergic reactions, while gut microbes transplanted from infants allergic to milk did not. The work, described online today in Nature Medicine, was supported in part by NIH’s National Institute of Allergy and Infectious Diseases. The findings may inform research to develop microbiome-based therapies to prevent or treat food allergy.

Scientists previously found that infants allergic to cow’s milk had different compositions of gut microbes than non-allergic infants. Previous studies also revealed that some microbes are associated with a lower risk of developing food allergy, leading researchers to examine whether gut microbes of infants without milk allergy might be protective.

Researchers transplanted gut microbes from each of eight infant donors into groups of mice raised in a sterile environment and sensitized to milk protein–meaning the animals’ immune systems created allergic antibodies to milk. When later exposed to milk, mice receiving no microbes or microbes from milk-allergic children produced allergic antibodies and experienced anaphylaxis, a potentially life-threatening allergic reaction. Mice receiving gut microbes from non-allergic infants had no reactions.

Investigators then analyzed microbes in infant stool samples, finding many differences between the stool of infants who were allergic to milk and those who were not. Mice transplanted with microbes from non-allergic infants also harbored a family of microbes previously found to protect against developing food allergies. Further experiments identified one microbe, Anaerostipes caccae, that prevented the development of milk allergy when transplanted alone into groups of mice. Researchers then sampled cells along the mice’s gut linings–where food allergies in mice and humans begin to develop. They found that mice that received microbes from non-allergic infants expressed different genes compared to those that did not, suggesting that microbes residing in the gut impact the host’s immune system. The researchers conclude that intestinal microbes play a critical role in regulating allergic responses to food and suggest that further research could lead to microbiome-modifying therapies to prevent or treat food allergy.

###

ARTICLE:

T Feehley et al. Healthy infants harbor intestinal bacteria that protect against food allergy. Nature Medicine DOI: 10.1038/s41591-018-0324-z (2019).

WHO:

Alkis Togias, M.D., chief of the Allergy, Asthma, and Airway Biology Branch in NIAID’s Division of Allergy, Immunology, and Transplantation, and Wendy Davidson, Ph.D., a program officer in the same branch, are available for comment.

CONTACT:

To schedule interviews, please contact Judith Lavelle, (301) 402-1663, niaidnews@niaid.nih.gov.

NIAID conducts and supports research–at NIH, throughout the United States, and worldwide–to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the HNIAID website.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov/.

Media Contact
Judith Lavelle
judith.lavelle@nih.gov
301-402-1663

Related Journal Article

http://dx.doi.org/10.1038/s41591-018-0324-z

Comments