Understanding sex differences in the allergic immune response to food.

Food allergies are of great public health concern due to their rising prevalence. Our understanding of how the immune system reacts to food remains incomplete. Allergic responses vary between individuals with food allergies. This variability could be caused by genetic, environmental, hormonal, or metabolic factors that impact immune responses mounted against allergens found in foods. Peanut (PN) allergy is one of the most severe and persistent of food allergies, warranting examination into how sensitization occurs to drive IgE-mediated allergic reactions. In recent years, much has been learned about the mechanisms behind the initiation of IgE-mediated food allergies, but additional questions remain. One unresolved issue is whether sex hormones impact the development of food allergies. Sex differences are known to exist in other allergic diseases, so this poses the question about whether the same phenomenon is occurring in food allergies. Studies show that females exhibit a higher prevalence of atopic conditions, such as allergic asthma and eczema, relative to males. Discovering such sex differences in allergic diseases provide a basis for investigating the mechanisms of how hormones influence the development of IgE-mediated reactions to foods. Analysis of existing food allergy demographics found that they occur more frequently in male children and adult females, which is comparable to allergic asthma. This paper reviews existing allergic mechanisms, sensitization routes, as well as how sex hormones may play a role in how the immune system reacts to common food allergens such as PN.

Allergic sensitization to peanuts is enhanced in mice fed a high-fat diet.

The incidence of peanut (PN) allergy is on the rise. As peanut allergy rates have continued to climb over the past few decades, obesity rates have increased to record highs, suggesting a link between obesity and the development of peanut allergy. While progress has been made, much remains to be learned about the mechanisms driving the development of allergic immune responses to peanut. Remaining unclear is whether consuming a Western diet, a diet characterized by overeating foods rich in saturated fat, salt, and refined sugars, supports the development of PN allergy. To address this, we fed mice a high fat diet to induce obesity. Once diet-induced obesity was established, mice were exposed to PN flour via the airways using our 4-week inhalation model. Mice were subsequently challenged with PN extract to induce anaphylaxis. Mice fed a high-fat diet developed significantly higher titers of PN-specific IgE, as well as stronger anaphylactic responses, when compared to their low-fat diet fed counterparts. These results suggest that obesity linked to eating a high-fat diet promotes the development of allergic immune responses to PN in mice. Such knowledge is critical to advance our growing understanding of the immunology of PN allergy.