Abstract
Impairment of the intestinal barrier is one of the key events in the initiation of the sensitization process in food allergy. The aim of this study was to explore the effects of kiwifruit allergen Act d 1 on intestinal permeability and tight junction protein (TJP) gene expression in vivo and to explore its potential to activate the NF-ĸB signaling pathway and to regulate expression of epithelial pro-allergenic cytokines. Influences of Act d 1 on TJP gene expression and pro-allergenic cytokines in the mouse intestine was analyzed by qPCR upon allergen administration by oral gavage. The effect on the in vivo intestinal permeability was assessed in ELISA by measuring the translocation of β-lactoglobulin (BLG) into circulation. The capacity of Act d 1 to activate the NF-ĸB pathway was tested in HEK293 cells by fluorescent microscopy and flow cytometry. Administration of Actinidin (Act d 1) increased intestinal permeability to the BLG. This was accompanied by changes in gene expression of TJP mRNA and pro-allergenic cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) compared to the control. Act d 1 reduced TEER of the HEK293 monolayer, was positive in an NF-ĸB-reporter HEK293 cell assay, and induced secretion of TSLP. These findings shed more light on the molecular events in the sensitization process of kiwifruit but possibly also of other protease food allergens.
Highlights
The prevalence of food allergies has significantly increased and become a substantial health burden in developed countries [1]
In murine models of food allergy, oral exposure to antigen and an adjuvant stimulates gut epithelial cells to express the innate pro-allergenic IL-33, IL-25, and thymic stromal lymphopoietin (TSLP), which contribute to the development of acute reactions to food and promotion of Th2 response [1,6,7,8]
Proteolytic activity of Act d 1 preparation was tested in a protease enzymatic assay with casein as a substrate (Figure 1)
Summary
The prevalence of food allergies has significantly increased and become a substantial health burden in developed countries [1]. One of the main mechanisms underlying food allergy involves the breakdown of the GI barrier and immunological tolerance against ingested food allergens [1,3]. A pivotal role of the GI barrier is the maintenance of intestinal homeostasis and the first line of defense against various mechanical, chemical, and microbial stressors from the environment, including natural antigens occurring in food [4]. In murine models of food allergy, oral exposure to antigen and an adjuvant stimulates gut epithelial cells to express the innate pro-allergenic IL-33, IL-25, and thymic stromal lymphopoietin (TSLP), which contribute to the development of acute reactions to food and promotion of Th2 response [1,6,7,8]
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