Frontiers in Allergy (Jun 2023)

GliSODin® prevents airway inflammation by inhibiting T-cell differentiation and activation in a mouse model of asthma

  • Martin Klein,
  • Eleonore Dijoux,
  • Marie-Aude Cheminant,
  • Laurent Intes,
  • Grégory Bouchaud

DOI
https://doi.org/10.3389/falgy.2023.1199355
Journal volume & issue
Vol. 4

Abstract

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BackgroundAsthma is a chronic inflammatory airway disease characterized by a prevailing type 2 inflammation, airway hyperresponsiveness, and mucus hypersecretion and is driven by various factors among which oxidative molecules, called reactive oxygen species (ROS), play a major role. Superoxide dismutases (SODs) are enzymes that constitute the first line of defense against ROS. Melon SOD-gliadin, which is known as GliSODin®, is commonly used as a nutritional supplement that has proven antioxidant properties.ObjectivesIn this study, we evaluated the efficacy and mechanism of action GliSODin® in the treatment of allergic asthma.MethodsHouse dust mite (HDM)-induced asthmatic mice were orally exposed to GliSODin®, and airway hyperresponsiveness, lung inflammation, in vitro T-cell polarization, in vivo T-cell reactivation, and blood immunoglobulin were investigated.ResultsGliSODin® reduced airway hyperresponsiveness, lung innate and adaptive immune response, and HDM-specific IgE production. Coculturing CD4+ T-cell with HDM-sensitized dendritic cells and GliSODin® reduced T-cell polarization into Th2 and Th17 cells. Moreover, adoptively transferred CD4+ T cells from asthmatic mice exhibited a reduced reactivation of Th2 and Th17 cells following stimulation with HDM plus GliSODin®.ConclusionGliSODin® abrogates asthma features and reduces CD4+ T-cell polarization and reactivation. Taken together, these data suggest that GliSODin® could be used for the management of asthma symptoms.

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