Effect of diet-induced obesity on ovalbumin-specific immune response in a murine asthma model☆
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Cited by (65)
Platycoside E alleviates allergic airway inflammation in obesity-related asthma mouse model
2023, Molecular ImmunologyTumor microenvironment metabolites directing T cell differentiation and function
2022, Trends in ImmunologyCitation 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].
Allergic asthma aggravated atherosclerosis increases cholesterol biosynthesis and foam cell formation in apolipoprotein E-deficient mice
2019, Biochemical and Biophysical Research CommunicationsObesity and asthma: What have we learned from animal models?
2018, Mechanisms and Manifestations of Obesity in Lung DiseaseObesity risk class and asthma outpatient service utilization by the middle aged and elderly in Taiwan
2016, Health PolicyCitation 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].
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Supported in part by a grant from the Japan Society of Home Economics, and by the Meji Life Welfare Group.