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133361 - High fat diet inhibits dendritic cell and T cell response to allergens but does not impair inhalational respiratory tolerance.pdf (721.72 kB)

High fat diet inhibits dendritic cell and T cell response to allergens but does not impair inhalational respiratory tolerance

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posted on 2023-05-20, 04:46 authored by Pizzolla, A, Oh, DY, Luong, S, Prickett, SR, Darren HenstridgeDarren Henstridge, Febbraio, MA, O'Hehir, RE, Rolland, JM, Hardy, CL
The incidence of obesity has risen to epidemic proportions in recent decades, most commonly attributed to an increasingly sedentary lifestyle, and a 'western' diet high in fat and low in fibre. Although non-allergic asthma is a well-established co-morbidity of obesity, the influence of obesity on allergic asthma is still under debate. Allergic asthma is thought to result from impaired tolerance to airborne antigens, so-called respiratory tolerance. We sought to investigate whether a diet high in fats affects the development of respiratory tolerance. Mice fed a high fat diet (HFD) for 8 weeks showed weight gain, metabolic disease, and alteration in gut microbiota, metabolites and glucose metabolism compared to age-matched mice fed normal chow diet (ND). Respiratory tolerance was induced by repeated intranasal (i.n.) administration of ovalbumin (OVA), prior to induction of allergic airway inflammation (AAI) by sensitization with OVA in alum i.p. and subsequent i.n. OVA challenge. Surprisingly, respiratory tolerance was induced equally well in HFD and ND mice, as evidenced by decreased lung eosinophilia and serum OVA-specific IgE production. However, in a pilot study, HFD mice showed a tendency for impaired activation of airway dendritic cells and regulatory T cells compared with ND mice after induction of respiratory tolerance. Moreover, the capacity of lymph node cells to produce IL-5 and IL-13 after AAI was drastically diminished in HFD mice compared to ND mice. These results indicate that HFD does not affect the inflammatory or B cell response to an allergen, but inhibits priming of Th2 cells and possibly dendritic cell and regulatory T cell activation.

History

Publication title

PLoS ONE

Volume

11

Issue

8

Pagination

e0160407

ISSN

1932-6203

Department/School

School of Health Sciences

Publisher

Public Library of Science

Place of publication

United States

Rights statement

Copyright 2016 Pizzolla et al. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/

Repository Status

  • Open

Socio-economic Objectives

Clinical health not elsewhere classified

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