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Molecular Mechanisms and Treatment of Allergic Reactions

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 5016

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Prof. Dr. Lucy C. Fairclough

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Guest Editor

School of Life Sciences, University of Nottingham, Nottingham, UK
Interests: immune mechanisms; allergic sensitization; immunology

Special Issue Information

Dear Colleagues,

Type I hypersensitivity is the most common form of allergy, comprising an IgE-mediated allergic reaction to a harmless substance, such as pollen, peanuts, and bee venom. In predisposed individuals, exposure to certain allergens results in the rapid onset of symptoms, and in extreme cases can be fatal. The prevalence of type I hypersensitivities has been increasing for decades, now affecting up to 40% of the population; thus, the need for advancements in treatment and a better understanding of the underlying mechanisms surrounding allergy development is crucial. This Special Issue focuses on the molecular mechanisms underlying type I hypersensitivity and developments in treatment options, contributing to an increased understanding of allergy and providing insights to guide future allergy treatment.

We warmly welcome submissions, including original investigations and review articles, on this topic.

Prof. Dr. Lucy C. Fairclough
Guest Editor

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Keywords

allergy
IgE
molecular mechanisms

Published Papers (5 papers)

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Research

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16 pages, 2427 KiB

Open AccessArticle

Glutenin from the Ancient Wheat Progenitor Is Intrinsically Allergenic as It Can Clinically Sensitize Mice for Systemic Anaphylaxis by Activating Th2 Immune Pathway

by Rick Jorgensen, Tamil Selvan Arul Arasan, Maya Blanka Srkalovic, Chris Van Antwerp, Perry K. W. Ng and Venu Gangur

Int. J. Mol. Sci. 2024, 25(13), 7324; https://doi.org/10.3390/ijms25137324 - 3 Jul 2024

Viewed by 569

Abstract

Wheat allergy is a major type of food allergy with the potential for life-threatening anaphylactic reactions. Common wheat, Triticum aestivum (hexaploid, AABBDD genome), was developed using tetraploid wheat (AABB genome) and the ancient diploid wheat progenitor (DD genome)-Aegilops tauschii. The potential allergenicity of gluten from ancient diploid wheat is unknown. In this study, using a novel adjuvant-free gluten allergy mouse model, we tested the hypothesis that the glutenin extract from this ancient wheat progenitor will be intrinsically allergenic in this model. The ancient wheat was grown, and wheat berries were used to extract the glutenin for testing. A plant protein-free colony of Balb/c mice was established and used in this study. The intrinsic allergic sensitization potential of the glutenin was determined by measuring IgE response upon transdermal exposure without the use of an adjuvant. Clinical sensitization for eliciting systemic anaphylaxis (SA) was determined by quantifying the hypothermic shock response (HSR) and the mucosal mast cell response (MMCR) upon intraperitoneal injection. Glutenin extract elicited a robust and specific IgE response. Life-threatening SA associated and a significant MMCR were induced by the glutenin challenge. Furthermore, proteomic analysis of the spleen tissue revealed evidence of in vivo Th2 pathway activation. In addition, using a recently published fold-change analysis method, several immune markers positively and negatively associated with SA were identified. These results demonstrate for the first time that the glutenin from the ancient wheat progenitor is intrinsically allergenic, as it has the capacity to elicit clinical sensitization for anaphylaxis via activation of the Th2 pathway in vivo in mice. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Allergic Reactions)

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14 pages, 3286 KiB

Open AccessArticle

Structural and Immunological Features of PR-10 Allergens: Focusing on the Major Alder Pollen Allergen Aln g 1

by Daria N. Melnikova, Ekaterina I. Finkina, Andrey E. Potapov, Yulia D. Danilova, Ilia Y. Toropygin, Natalia S. Matveevskaya, Tatiana V. Ovchinnikova and Ivan V. Bogdanov

Int. J. Mol. Sci. 2024, 25(9), 4965; https://doi.org/10.3390/ijms25094965 - 2 May 2024

Viewed by 767

Abstract

Today, allergies have become a serious problem. PR-10 proteins are clinically relevant allergens that have the ability to bind hydrophobic ligands, which can significantly increase their allergenicity potential. It has been recently shown that not only the birch pollen allergen Bet v 1 but also the alder pollen allergen Aln g 1, might act as a true sensitizer of the immune system. The current investigation is aimed at the further study of the allergenic and structural features of Aln g 1. By using qPCR, we showed that Aln g 1 was able to upregulate alarmins in epithelial cells, playing an important role in sensitization. With the use of CD-spectroscopy and ELISA assays with the sera of allergic patients, we demonstrated that Aln g 1 did not completely restore its structure after thermal denaturation, which led to a decrease in its IgE-binding capacity. Using site-directed mutagenesis, we revealed that the replacement of two residues (Asp27 and Leu30) in the structure of Aln g 1 led to a decrease in its ability to bind to both IgE from sera of allergic patients and lipid ligands. The obtained data open a prospect for the development of hypoallergenic variants of the major alder allergen Aln g 1 for allergen-specific immunotherapy. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Allergic Reactions)

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16 pages, 2926 KiB

Open AccessArticle

Severe Type 2 Inflammation Leads to High Platelet-Activating-Factor-Associated Pathology in Chronic Rhinosinusitis with Nasal Polyps—A Hierarchical Cluster Analysis Using Bulk RNA Barcoding and Sequencing

by Takashi Ishino, Takashi Oda, Tomohiro Kawasumi, Kota Takemoto, Manabu Nishida, Yuichiro Horibe, Nobuyuki Chikuie, Takayuki Taruya, Takao Hamamoto, Tsutomu Ueda and Sachio Takeno

Int. J. Mol. Sci. 2024, 25(4), 2113; https://doi.org/10.3390/ijms25042113 - 9 Feb 2024

Viewed by 1008

Abstract

Platelet-activating factor (PAF) is a phospholipid-derived inflammatory mediator that triggers various inflammatory conditions, including eosinophil activation and recruitment. This study aimed to evaluate the expressions of PAF-metabolism-associated genes, namely genes coding the enzymes involved in PAF synthesis (LPCAT1, LPCAT2, LPCAT3, and LPCAT4), PAF degradation (PAFAH1B2, PAFAH1B3, and PAFAH2), and the gene for the PAF receptor (PTAFR) in subtypes of CRSwNP classified by clinical- or hierarchal-analysis-based classifications. Transcriptomic analysis using bulk RNA barcoding and sequencing (BRB-seq) was performed with CRSwNP, including eosinophilic CRS (ECRS) (n = 9), nonECRS (n = 8), ECRS with aspirin-exacerbated respiratory disease (Asp) (n = 3), and controls with a normal uncinate process mucosa (n = 6). PTAFR was only upregulated in ECRS and nonECRS. In the hierarchical cluster analysis with clusters 1 and 2 reflecting patients with low-to-moderate and high levels of type 2 inflammation, respectively, cluster 1 exhibited a significant downregulation of LPCAT2 and an upregulation of PTAFR expression, while cluster 2 showed an upregulation of LPCAT1, PAFAH1B2, and PTAFR and downregulation of PAFAH2 expression. Understanding this strong PAF-associated pathophysiology in the severe type 2 inflammation group could provide valuable insights into the treatment and management of CRSwNP. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Allergic Reactions)

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Review

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20 pages, 1374 KiB

Open AccessReview

Deciphering the Interplay between the Epithelial Barrier, Immune Cells, and Metabolic Mediators in Allergic Disease

by Lea Ling-Yu Kan, Peiting Li, Sharon Sze-Man Hon, Andrea Yin-Tung Lai, Aixuan Li, Katie Ching-Yau Wong, Danqi Huang and Chun-Kwok Wong

Int. J. Mol. Sci. 2024, 25(13), 6913; https://doi.org/10.3390/ijms25136913 - 24 Jun 2024

Viewed by 633

Abstract

Chronic exposure to harmful pollutants, chemicals, and pathogens from the environment can lead to pathological changes in the epithelial barrier, which increase the risk of developing an allergy. During allergic inflammation, epithelial cells send proinflammatory signals to group 2 innate lymphoid cell (ILC2s) and eosinophils, which require energy and resources to mediate their activation, cytokine/chemokine secretion, and mobilization of other cells. This review aims to provide an overview of the metabolic regulation in allergic asthma, atopic dermatitis (AD), and allergic rhinitis (AR), highlighting its underlying mechanisms and phenotypes, and the potential metabolic regulatory roles of eosinophils and ILC2s. Eosinophils and ILC2s regulate allergic inflammation through lipid mediators, particularly cysteinyl leukotrienes (CysLTs) and prostaglandins (PGs). Arachidonic acid (AA)-derived metabolites and Sphinosine-1-phosphate (S1P) are significant metabolic markers that indicate immune dysfunction and epithelial barrier dysfunction in allergy. Notably, eosinophils are promoters of allergic symptoms and exhibit greater metabolic plasticity compared to ILC2s, directly involved in promoting allergic symptoms. Our findings suggest that metabolomic analysis provides insights into the complex interactions between immune cells, epithelial cells, and environmental factors. Potential therapeutic targets have been highlighted to further understand the metabolic regulation of eosinophils and ILC2s in allergy. Future research in metabolomics can facilitate the development of novel diagnostics and therapeutics for future application. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Allergic Reactions)

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14 pages, 1262 KiB

Open AccessReview

The Role of Extracellular Vesicles in Atopic Dermatitis

by Catherine Harvey-Seutcheu, Georgina Hopkins and Lucy C. Fairclough

Int. J. Mol. Sci. 2024, 25(6), 3255; https://doi.org/10.3390/ijms25063255 - 13 Mar 2024

Viewed by 1554

Abstract

Atopic dermatitis, or eczema, is the most common chronic skin disorder, characterized by red and pruritic lesions. Its etiology is multifaceted, involving an interplay of factors, such as the allergic immune response, skin barrier dysfunction, and dysbiosis of the skin microbiota. Recent studies have explored the role of extracellular vesicles (EVs), which are lipid bilayer-delimitated particles released by all cells, in atopic dermatitis. Examination of the available literature identified that most studies investigated EVs released by Staphylococcus aureus, which were found to impact the skin barrier and promote the release of cytokines that contribute to atopic dermatitis development. In addition, EVs released by the skin fungus, Malassezia sympodialis, were found to contain allergens, suggesting a potential contribution to allergic sensitization via the skin. The final major finding was the role of EVs released by mast cells, which were capable of activating various immune cells and attenuating the allergic response. While research in this area is still in its infancy, the studies examined in this review provide encouraging insights into how EVs released from a variety of cells play a role in both contributing to and protecting against atopic dermatitis. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Allergic Reactions)

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