Elsevier

Metabolism

Volume 51, Issue 10, October 2002, Pages 1241-1246
Metabolism

Effect of diet-induced obesity on ovalbumin-specific immune response in a murine asthma model

https://doi.org/10.1053/meta.2002.35196Get rights and content

Abstract

Some epidemiologic surveys have demonstrated that asthma is more prevalent in obese children and adults. However, the mechanism of association between obesity and asthma has not been fully clarified. This report investigates a murine model for antigen-induced asthma and diet-induced obesity from an immunologic perspective. For the induction of obesity, C57BL/6J mice were fed a high-fat diet supplemented with lard or soybean oil. Mice were then sensitized and challenged with ovalbumin (OVA) to induce allergic lung inflammation. OVA-specific serum immunoglobulin levels were lower in obese mice compared with non-obese control mice. The decline of OVA-specific IgE in the soybean oil group was found to be especially pronounced. However, obese mice with OVA-induced asthma showed a higher sensitivity of antigen-induced T-cell responses, and increased gamma interferon (IFN-[gamma ]) production of splenocytes with phytohemagglutinin (PHA) stimulation. Furthermore, mast cell numbers in the tracheal mucosa were increased in obese mice upon sensitization by OVA. These results suggest that obesity-induced changes in T-cell function may be partly involved in the pathophysiology of asthma in human obesity, rather than Ig E-mediated allergic responses.

References (0)

Cited by (65)

  • Tumor microenvironment metabolites directing T cell differentiation and function

    2022, Trends in Immunology
    Citation Excerpt :

    However, low and non-toxic concentrations of FAs may suppress T cell activation to varying degrees, depending on the stimulus used for T cell activation; this was evidenced from palmitic acid studies showing it suppresses concanavalin A-induced T cell proliferation, but not T cells with anti-CD3 antibody stimulation, in vitro [16,18,21]. High-FA diets in rats can suppress splenic T cell proliferation, due to the presence of oils rich in saturated FAs, monounsaturated FAs, n-6 polyunsaturated fatty acids (PUFA), or n-3 PUFA in diets [22,23]. Cholesterol can also alter T cell proliferation and dietary-induced hypercholesterolemia can enhance T cell receptor (TCR)-stimulated T cell proliferation and increase TCR signaling strength in CD4+ T cells, as evidenced from the increased expression of transcription factor Nur77 [24].

  • Obesity and asthma: What have we learned from animal models?

    2018, Mechanisms and Manifestations of Obesity in Lung Disease
  • Obesity risk class and asthma outpatient service utilization by the middle aged and elderly in Taiwan

    2016, Health Policy
    Citation Excerpt :

    Many epidemiological studies have examined and confirmed the relationship between these risk factors and asthma [3–16]. The relationship of one of these risk factors in particular, obesity, with asthma has drawn attention to public health trends in recent decades [4–10,12,13,17–25]. Studies have found obesity is associated with asthma, and there is a growing evidence for the existence of a causal association and may significantly affect asthma risk and phenotype [26,27].

View all citing articles on Scopus

Supported in part by a grant from the Japan Society of Home Economics, and by the Meji Life Welfare Group.

View full text