An Evaluation of the Mechanisms of Galacto-Oligosaccharide (GOS)-Induced IgE Cross-Linking on Basophils in GOS Allergy

Abstract

The prebiotics, galacto-oligosaccharides (GOS), are small carbohydrate molecules with 1–7 galactose units linked to glucose and have been shown to trigger IgE-mediated anaphylaxis in some cases following ingestion. It is still an unresolved question of how GOS cross-links IgE on basophils. In this study, we examined whether human galectins, a class of lectins that bind specifically to β-galactoside carbohydrates, are involved in GOS-induced basophil activation. Basophil activation test to GOS and control allergen, Blomia tropicalis (Blo t) extract were performed in the presence or absence of four sugar-based galectin inhibitors (lactose, thiodigalactoside [TDG], TD139, and GB1107) and one peptide-based inhibitor, G3-C12. Results showed that TD139, GB1107, and G3-C12 did not display a specific inhibitory effect on GOS-induced basophil activation as compared to control allergen. An inhibitory effect of lactose and TDG on GOS-induced basophil activation was observed and varied between subjects with up to 100% inhibition at low doses of GOS. The results of competitive ELISA suggest that the inhibitory effects of high dose lactose and TDG on the basophil activation is likely due to the cross-reactivity of GOS-specific IgE to lactose and TDG. Basophil activation is performed using purified basophils suggested that cell surface receptors on other blood cells were not required to induce basophil activation. In conclusion, our results suggest that GOS, a low molecular weight sugar, is able to cross-link IgE independently.

New developments in biotechnology applied to microorganisms

“…Possible issues for the GMM risk assessment are related to: (i) allergenicity and adjuvanticity of proteins; (ii) carbohydrates; (iii) other substances produced by GMMs; (iv) altered protein secretion by GMMs, or those derived from their metabolism; (v) GMM functionality (e.g. ability to induce allergic sensitisation or conditions prone to it); and (vi) non‐IgE‐mediated allergy to proteins such as eosinophilic esophagitis or other gastrointestinal disorders (Akdis, 2021 ; Caminero et al., 2023 ; EFSA GMO Panel, 2017 ; Hang et al., 2019 ; Le Gall et al., 2011 ; Lee et al., 2022 ; Levan et al., 2019 ; Lloyd‐Price et al., 2019 ; Platts‐Mills et al., 2021 ; Plum et al., 2023 ; Sharma & Karim, 2021 ; Sozener et al., 2022 ). In allergic disease, adjuvants alter tissue homeostasis to establish conditions that result in non‐specific, innate type 2 (allergic) priming to bystander allergens, thus subverting the development of tolerance (Akdis, 2021 ; Bruton et al., 2020 ; Ellenbogen et al., 2018 ; Kopp et al., 2023 ).…”