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      Dietary Fiber and Bacterial SCFA Enhance Oral Tolerance and Protect against Food Allergy through Diverse Cellular Pathways.

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          Abstract

          The incidence of food allergies in western countries has increased dramatically in recent decades. Tolerance to food antigens relies on mucosal CD103(+) dendritic cells (DCs), which promote differentiation of regulatory T (Treg) cells. We show that high-fiber feeding in mice improved oral tolerance and protected from food allergy. High-fiber feeding reshaped gut microbial ecology and increased the release of short-chain fatty acids (SCFAs), particularly acetate and butyrate. High-fiber feeding enhanced oral tolerance and protected against food allergy by enhancing retinal dehydrogenase activity in CD103(+) DC. This protection depended on vitamin A in the diet. This feeding regimen also boosted IgA production and enhanced T follicular helper and mucosal germinal center responses. Mice lacking GPR43 or GPR109A, receptors for SCFAs, showed exacerbated food allergy and fewer CD103(+) DCs. Dietary elements, including fiber and vitamin A, therefore regulate numerous protective pathways in the gastrointestinal tract, necessary for immune non-responsiveness to food antigens.

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          Author and article information

          Journal
          Cell Rep
          Cell reports
          Elsevier BV
          2211-1247
          Jun 21 2016
          : 15
          : 12
          Affiliations
          [1 ] Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia.
          [2 ] School of Medicine, Deakin University, Waurn Ponds, VIC 3216, Australia.
          [3 ] Department of Molecular Cell Biology and Immunology, VU University Medical Center, 1081 HZ Amsterdam, the Netherlands.
          [4 ] Department of Pathogens and Immunity, John Curtin School of Medical Research, Australian National University, Building 131, Garran Road, Canberra, ACT 0200, Australia.
          [5 ] Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia; Charles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia; Department of Physiology, Faculty of Medicine, The University of Sydney, Sydney, NSW 2006, Australia. Electronic address: laurence.macia@sydney.edu.au.
          [6 ] Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia; Charles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia; Department of Physiology, Faculty of Medicine, The University of Sydney, Sydney, NSW 2006, Australia. Electronic address: charles.mackay@monash.edu.
          Article
          S2211-1247(16)30630-1
          10.1016/j.celrep.2016.05.047
          27332875
          64c44c0c-bb68-413c-89bc-02164cb12b59
          History

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