Abstract
In his correspondence, Turner1 argues that factors other than increased intestinal permeability contribute to heightened food allergen absorption in humans prone to severe allergic reactions and anaphylaxis. He notes that there is a lack of evidence supporting the role of heightened intestinal permeability in mediating symptomatic food allergy in humans, and that gut-barrier dysfunction may be a result of allergic inflammation, rather than a cause. These critiques highlight both the challenges of studying food allergy in humans and the need to understand differences that may exist in food allergy pathogenesis between humans and mice.
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