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

Hussain, Maryam; Bonilla-Rosso, Germán; Kwong Chung, Cheong K. C.; Bäriswyl, Lukas; Rodriguez, Maria Pena; Kim, Brian S; Engel, Philipp; Noti, Mario (2019). High dietary fat intake induces a microbiota signature that promotes food allergy. Journal of allergy and clinical immunology, 144(1), 157-170.e8. Elsevier 10.1016/j.jaci.2019.01.043

[img] Text
1-s2.0-S0091674919302052-main.pdf - Published Version
Restricted to registered users only
Available under License Publisher holds Copyright.

Download (4MB) | Request a copy
[img]
Preview
Text
YMAI_13890_edit_report (1).pdf - Accepted Version
Available under License Creative Commons: Attribution-Noncommercial-No Derivative Works (CC-BY-NC-ND).

Download (2MB) | Preview

BACKGROUND

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.

OBJECTIVE

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.

METHODS

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.

RESULTS

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.

CONCLUSION

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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Service Sector > Institute of Pathology > Immunopathology

Graduate School:

Graduate School for Cellular and Biomedical Sciences (GCB)

UniBE Contributor:

Hussain, Maryam, Kwong Chung, Cheong Kwet Choy, Bäriswyl, Lukas, Noti, Mario

ISSN:

1097-6825

Publisher:

Elsevier

Language:

English

Submitter:

Christa Hagert

Date Deposited:

13 Nov 2019 14:59

Last Modified:

05 Dec 2022 15:32

Publisher DOI:

10.1016/j.jaci.2019.01.043

PubMed ID:

30768991

Uncontrolled Keywords:

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

BORIS DOI:

10.7892/boris.134745

URI:

https://boris.unibe.ch/id/eprint/134745

Actions (login required)

Edit item Edit item
Provide Feedback