NEW research on immunoglobulin E (IgE)-mediated anaphylaxis suggests that food allergy severity may depend not only on the immune system, but also on how bacteria in saliva and the small intestine metabolise allergens.
In a series of mechanistic and clinical experiments, researchers found that specific oral and small intestinal microbes were capable of degrading peanut allergens before they triggered severe allergic reactions. The findings suggested that microbial metabolism directly influenced the intensity of IgE-mediated anaphylaxis, offering a potential new avenue for reducing risk in patients with peanut allergy.
Food-induced anaphylaxis is an acute, potentially life-threatening systemic reaction driven largely by IgE antibodies, which bind allergens and activate mast cells. Peanut allergy remains one of the most common and severe causes, with reactions ranging from urticaria to cardiovascular collapse. While the human microbiota has previously been linked to oral tolerance, its direct role in shaping IgE-mediated responses has been unclear.
Human Microbiota Degrade Peanut Allergens
The investigators demonstrated that human saliva and jejunal samples harboured peanut-degrading bacteria capable of metabolising the immunodominant allergens Ara h 1 and Ara h 2. In vitro experiments showed that isolated Rothia and Staphylococcus species broke down these allergens into fragments with reduced IgE binding capacity and diminished mast cell activation.
In mouse models colonised with Rothia, levels of intact Ara h 1 and Ara h 2 in both local intestinal tissue and systemic circulation were significantly lower following peanut challenge. These mice experienced attenuated anaphylaxis compared with controls, indicating that microbial allergen metabolism limited both allergen absorption and downstream immune activation.
Clinical Links Between Microbes and Anaphylaxis Risk
Importantly, the translational arm of the study analysed samples from patients with peanut allergy. Individuals with higher abundance of common peanut-degrading bacteria, including Rothia, exhibited a higher threshold for allergic reactions during controlled exposure. This suggested that microbial composition may help explain variability in anaphylaxis severity among patients with similar IgE profiles.
The data collectively supports a model in which gut microbiota actively modulate IgE-mediated anaphylaxis by enzymatically transforming food allergens before systemic absorption.
These findings raised the possibility that microbiota-targeted therapies, such as probiotics or microbial enzyme supplementation, could complement existing strategies for peanut allergy management. Further clinical trials will be required to determine whether modifying allergen-degrading bacterial populations can meaningfully reduce the risk or severity of IgE-mediated anaphylaxis in clinical practice.
Reference
Sánchez-Martínez E et al. Microbial metabolism of food allergens determines the severity of IgE-mediated anaphylaxis. Cell Host Microbe. 2026; DOI:10.1016/j.chom.2026.02.013.
Featured image: Q STOCK on Adobe Stock
