Dysfunctional microbiota with reduced capacity to produce butyrate as a basis for allergic diseases

• Published in: Journal of allergy and clinical immunology Vol. 144; no. 6; pp. 1513 - 1515
• Main Authors: Macia, Laurence, Mackay, Charles R.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2019; Elsevier Limited
• Subjects: Acetic acid; Age; Allergic diseases; allergy; Antibiotics; Antigens; Asthma; Atopy; Bacteria; butyrate; Butyrates; Carbohydrates; CAZymes; CD103 antigen; Children; Dendritic cells; Diet; Dietary fiber; Disease; Enzymes; Farming; Fermentation; Food allergies; Gastrointestinal Microbiome; Gut microbiota; Histone deacetylase; Humans; Hygiene; Hypersensitivity; Hypotheses; Immunological tolerance; Infant; Inflammatory diseases; Lymphocytes T; Microbiomes; Microbiota; Milk; Molecular modelling; Mucosa; Nutrition research; Prebiotics; Probiotics; Propionic acid; Respiratory tract diseases; Starch; United Kingdom > UK; Australia; United States > US; Gut microbiota; allergy; butyrate; dietary fiber; CAZymes
• ISSN: 0091-6749; 1097-6825; 1097-6825
• DOI: 10.1016/j.jaci.2019.10.009

In the 1-year-old microbiome they found that the total number of CAZyme genes in families that degrade plant cell-wall, animal, and fungal carbohydrates were depleted in children who became atopic relative to control subjects. [...]the microbiome of children who became atopic had less capacity to degrade the resistant starch in their diet also at 1 year. [...]it is striking that children with atopy have, from early stages of life, a dysfunctional microbiome with a poor ability to efficiently degrade complex carbohydrates derived either from milk or food. Butyrate and acetate were behind the beneficial effects of high fiber in a food allergy model in mice through their binding of GPR43 and GPR109a.6 Propionate and GPR41 are protective in mice with asthma-like allergic airway inflammation.10 SCFAs might also promote Treg cells through epigenetic changes caused by inhibition of histone deacetylases, with acetate protecting from asthma-like inflammatory diseases in mice through increases in Treg cell numbers caused by histone deacetylase 9.5 SCFAs promote Treg cells either directly by promoting peripheral Treg cell development from naive T cells or indirectly through effects on CD103+ dendritic cells (the master regulators of mucosal tolerance).6 A summary of all the cellular and molecular mechanisms that might be leading to allergy/asthma is presented in Fig 1.