Intestinal Barrier Permeability in Allergic Diseases

Niewiem, Monika; Grzybowska-Chłebowczyk, Urszula

doi:10.3390/nu14091893

Cited by 53 publications

(35 citation statements)

References 78 publications

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“…Food allergens can result in increased gut permeability and induce gut inflammation. Once the intestine is damaged, allergens will enter the peripheral circulation more smoothly, and will further intensify the allergic response [ 6 , 7 ]. In this study, we explored the efficacy of oral AVA on OVA-induced colonic injury in mice, and inquired about the possible mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…The pathogenesis of FA is characterized by the induction of T helper 2 (Th2) cell reaction induced by the disruption of oral tolerance to exogenous allergens [ 4 , 5 ]. It is worth noting that the overexposure to food allergens can result in the intestinal inflammation and mucosal barrier injury, which thus makes it easier for food allergens to enter the bloodstream, and then aggravates the allergic reaction and intestinal damage [ 6 , 7 ]. Therefore, it is necessary to explore effective strategies to relieve intestinal injury and inflammation induced by food antigens.…”

Section: Introductionmentioning

confidence: 99%

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Avenanthramide Improves Colonic Damage Induced by Food Allergies in Mice through Altering Gut Microbiota and Regulating Hsp70-NF-κB Signaling

et al. 2023

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Food allergies can cause intestinal damage that can exacerbate allergic symptoms, and gut microbiota have been shown to influence allergic development. This study was intended to investigate the effects of Avenanthramide (AVA) on colonic damage induced by food allergy and its mechanism. In Exp. 1, AVA administrations alleviated colonic inflammation in mice challenged with ovalbumin, as shown by decreased concentrations of TNF-α, IL-25 and IL-33. Additionally, the AVA supplementations improved intestinal barrier damage by elevating occludin, ZO-1 and claudin-1 levels. Moreover, AVA inhibited NF-κB phosphorylation and enhanced heat shock protein 70 (Hsp70) expression in the colon. In Exp. 2, apoptozole as a Hsp70 inhibitor was used to explore the Hsp70-NF-κB signaling contribution to AVA function. The AVA additions increased the productions of acetate and butyrate, but decreased propionate. Notably, AVA reduced the colonic abundance of propionate-producing microbes such as Muribaculaceae, but elevated butyrate-producing microbes including Roseburia, Blautia, and Lachnospiraceae_NK4A136_group. Microbial alteration could be responsible for the increased butyrate, and thus the up-regulated Hsp70. However, apoptozole treatment eliminated the effects of AVA. Our study revealed that AVA improved colonic injury and inflammation induced by food allergies, and this mechanism may be mediated by the increased microbial-derived butyrate and involved in the Hsp70-NF-κB signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Avenanthramide Improves Colonic Damage Induced by Food Allergies in Mice through Altering Gut Microbiota and Regulating Hsp70-NF-κB Signaling

et al. 2023

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“…The apical junction complexes (AJCs) are one of the main components maintaining the integrity of epithelial barriers as they regulate cell-cell adhesion, cell polarity, and paracellular permeability of exogenous elements. These complexes are composed of two main structures, the tight junctions (TJs) and the adherens junctions (AJs) ( 36 – 38 ). TJs are formed by extracellular domains of transmembrane proteins (such as occludin and claudin protein families) that form strong links between them and connect with actin and tubulin cytoskeleton via scaffold proteins such as zonula occludens -1 (ZO-1) ( 39 ).…”

Section: Epithelial Barriers Play a Key Role In Allergy Developmentmentioning

confidence: 99%

Beyond allergic progression: From molecules to microbes as barrier modulators in the gut-lung axis functionality

et al. 2023

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The “epithelial barrier hypothesis” states that a barrier dysfunction can result in allergy development due to tolerance breakdown. This barrier alteration may come from the direct contact of epithelial and immune cells with the allergens, and indirectly, through deleterious effects caused by environmental changes triggered by industrialization, pollution, and changes in the lifestyle. Apart from their protective role, epithelial cells can respond to external factors secreting IL-25 IL-33, and TSLP, provoking the activation of ILC2 cells and a Th2-biased response. Several environmental agents that influence epithelial barrier function, such as allergenic proteases, food additives or certain xenobiotics are reviewed in this paper. In addition, dietary factors that influence the allergenic response in a positive or negative way will be also described here. Finally, we discuss how the gut microbiota, its composition, and microbe-derived metabolites, such as short-chain fatty acids, alter not only the gut but also the integrity of distant epithelial barriers, focusing this review on the gut-lung axis.

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“…An increased intestinal permeability was found in patients with AD ( 68 ), AA ( 69 ), and FA ( 70 ). It was suggested that the dysregulation of claudin-1, claudin-4, claudin-5, and claudin-8 impairs intestinal barrier integrity and leads to the increased allergen penetration ( 71 , 72 ). Moreover, the disruption of occludin raises intestinal permeability of macro-particles ( 73 ), which may contribute to the increased allergen entry.…”

Section: The Epithelial Barrier In Atopic Disordersmentioning

confidence: 99%

Claudin-1 Mediated Tight Junction Dysfunction as a Contributor to Atopic March

Xia

Cao²,

Zheng³

2022

Front. Immunol.

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Atopic march refers to the phenomenon wherein the occurrence of asthma and food allergy tends to increase after atopic dermatitis. The mechanism underlying the progression of allergic inflammation from the skin to gastrointestinal (GI) tract and airways has still remained elusive. Impaired skin barrier was proposed as a risk factor for allergic sensitization. Claudin-1 protein forms tight junctions and is highly expressed in the epithelium of the skin, airways, and GI tract, thus, the downregulation of claudin-1 expression level caused by CLDN-1 gene polymorphism can mediate common dysregulation of epithelial barrier function in these organs, potentially leading to allergic sensitization at various sites. Importantly, in patients with atopic dermatitis, asthma, and food allergy, claudin-1 expression level was significantly downregulated in the skin, bronchial and intestinal epithelium, respectively. Knockdown of claudin-1 expression level in mouse models of atopic dermatitis and allergic asthma exacerbated allergic inflammation, proving that downregulation of claudin-1 expression level contributes to the pathogenesis of allergic diseases. Therefore, we hypothesized that the tight junction dysfunction mediated by downregulation of claudin-1 expression level contributes to atopic march. Further validation with clinical data from patients with atopic march or mouse models of atopic march is needed. If this hypothesis can be fully confirmed, impaired claudin-1 expression level may be a risk factor and likely a diagnostic marker for atopic march. Claudin-1 may serve as a valuable target to slowdown or block the progression of atopic march.

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Intestinal Barrier Permeability in Allergic Diseases

Cited by 53 publications

References 78 publications

Avenanthramide Improves Colonic Damage Induced by Food Allergies in Mice through Altering Gut Microbiota and Regulating Hsp70-NF-κB Signaling

Avenanthramide Improves Colonic Damage Induced by Food Allergies in Mice through Altering Gut Microbiota and Regulating Hsp70-NF-κB Signaling

Beyond allergic progression: From molecules to microbes as barrier modulators in the gut-lung axis functionality

Claudin-1 Mediated Tight Junction Dysfunction as a Contributor to Atopic March

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