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J Allergy Clin Immunol. 2019 Jul;144(1):157-170.e8. doi: 10.1016/j.jaci.2019.01.043. Epub 2019 Feb 13.

High dietary fat intake induces a microbiota signature that promotes food allergy.

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Institute of Pathology, Department of Experimental Pathology, University of Bern, Bern, Switzerland; Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland.
Department of Fundamental Microbiology, University of Lausanne, Lausanne, Switzerland.
Institute of Pathology, Department of Experimental Pathology, University of Bern, Bern, Switzerland.
Division of Dermatology, Department of Medicine, Washington University School of Medicine, St Louis, Mo.
Institute of Pathology, Department of Experimental Pathology, University of Bern, Bern, Switzerland. Electronic address:



Diet-induced obesity and food allergies increase in tandem, but a potential cause-and-effect relationship between these diseases of affluence remains to be tested.


We sought to test the role of high dietary fat intake, diet-induced obesity, and associated changes in gut microbial community structure on food allergy pathogenesis.


Mice were fed a high-fat diet (HFD) for 12 weeks before food allergen sensitization on an atopic dermatitis-like skin lesion, followed by intragastric allergen challenge to induce experimental food allergy. Germ-free animals were colonized with a signature HFD or lean microbiota for 8 weeks before induction of food allergy. Food-induced allergic responses were quantified by using a clinical allergy score, serum IgE levels, serum mouse mast cell protease 1 concentrations, and type 2 cytokine responses. Accumulation of intestinal mast cells was examined by using flow cytometry and chloroacetate esterase tissue staining. Changes in the gut microbial community structure were assessed by using high-throughput 16S ribosomal DNA gene sequencing.


HFD-induced obesity potentiates food-induced allergic responses associated with dysregulated intestinal effector mast cell responses, increased intestinal permeability, and gut dysbiosis. An HFD-associated microbiome was transmissible to germ-free mice, with the gut microbial community structure of recipients segregating according to the microbiota input source. Independent of an obese state, an HFD-associated gut microbiome was sufficient to confer enhanced susceptibility to food allergy.


These findings identify HFD-induced microbial alterations as risk factors for experimental food allergy and uncouple a pathogenic role of an HFD-associated microbiome from obesity. Postdieting microbiome alterations caused by overindulgence of dietary fat might increase susceptibility to food allergy.


Food allergy; IgE; basophils; diet-induced obesity; dysbiosis; germ-free; high-fat diet; mast cells; microbiota


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