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Genetics and Epigenetics of Allergy Diseases
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Genetics and Epigenetics of Allergy Diseases

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Epigenomics".

Deadline for manuscript submissions: closed (1 March 2022) | Viewed by 19636

Special Issue Editors

Prof. Dr. Catalina Sanz

E-Mail Website
Guest Editor
Department of Microbiology and Genetics, University of Salamanca, 37007 Salamanca, Spain
Interests: genetics; epigenetics; allergy; gene regulation; pharmacogenomics
Prof. Dr. Asunción García-Sánchez

E-Mail Website
Guest Editor
Department of Biomedical Sciences and Diagnostics, University of Salamanca, 37007 Salamanca, Spain
Interests: molecular mechanisms of allergic diseases; molecular; human biology; medical genetics; regulation of gene expression; epigenetics

Special Issue Information

Dear Colleagues,

Allergic diseases are a clear example of complex multifactorial diseases mediated by the interaction of different genetic and epigenetic factors. Whole genome sequencing studies and polygenic risk score analyses in well-characterized homogeneous populations have provided a wealth of information on many susceptibility genes. However, many gene associations have not been able to be replicated, and functional studies on the mechanisms that mediate these diseases are still scarce. In this sense, epigenetic factors provide additional information that could explain not only the discrepancies observed between monozygotic twins but also phenomena such as incomplete penetrance, variable expression, gender and progenitor effects, and the progressive increase in the prevalence of allergic diseases observed during the last few decades. Different studies have shown a connection between disease susceptibility and environmental exposure during intrauterine life or early childhood, potentially mediated by epigenetic modifications. In response to an environmental challenge, epigenetic modifications allow an adaptive change that modifies gene expression and leads to the triggering of allergic diseases. In this Special Issue, different genetic and epigenetic factors involved in the development of allergic diseases will be considered.

Prof. Dr. Catalina Sanz
Dr. Asunción García-Sánchez
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • genetics of allergy
  • gene functional studies in allergy
  • epigenetic modifications in allergy
  • pharmacogenetics in allergy
  • gene therapies in allergy
  • interactions between genes and environment in allergies

Published Papers (5 papers)

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Research

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20 pages, 2833 KiB  
Article
Single-Cell RNA-Seq Analysis Reveals Lung Epithelial Cell Type-Specific Responses to HDM and Regulation by Tet1
by Tao Zhu, Anthony P. Brown, Lucy P. Cai, Gerald Quon and Hong Ji
Genes 2022, 13(5), 880; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13050880 - 14 May 2022
Cited by 5 | Viewed by 3419
Abstract
Tet1 protects against house dust mite (HDM)-induced lung inflammation in mice and alters the lung methylome and transcriptome. In order to explore the role of Tet1 in individual lung epithelial cell types in HDM-induced inflammation, we established a model of HDM-induced lung inflammation [...] Read more.
Tet1 protects against house dust mite (HDM)-induced lung inflammation in mice and alters the lung methylome and transcriptome. In order to explore the role of Tet1 in individual lung epithelial cell types in HDM-induced inflammation, we established a model of HDM-induced lung inflammation in Tet1 knockout and littermate wild-type mice, then studied EpCAM+ lung epithelial cells using single-cell RNA-seq analysis. We identified eight EpCAM+ lung epithelial cell types, among which AT2 cells were the most abundant. HDM challenge altered the relative abundance of epithelial cell types and resulted in cell type-specific transcriptomic changes. Bulk and cell type-specific analysis also showed that loss of Tet1 led to the altered expression of genes linked to augmented HDM-induced lung inflammation, including alarms, detoxification enzymes, oxidative stress response genes, and tissue repair genes. The transcriptomic regulation was accompanied by alterations in TF activities. Trajectory analysis supports that HDM may enhance the differentiation of AP and BAS cells into AT2 cells, independent of Tet1. Collectively, our data showed that lung epithelial cells had common and unique transcriptomic signatures of allergic lung inflammation. Tet1 deletion altered transcriptomic networks in various lung epithelial cells, which may promote allergen-induced lung inflammation. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Allergy Diseases)
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12 pages, 293 KiB  
Article
Polymorphisms in Human IL4, IL10, and TNF Genes Are Associated with an Increased Risk of Developing NSAID-Exacerbated Respiratory Disease
by María Luisa Reigada-Rivera, Catalina Sanz Lozano, Esther Moreno Rodilla, Asunción García-Sánchez, Virginia García-Solaesa, Félix Lorente Toledano, Ignacio Dávila González and María Isidoro-García
Genes 2022, 13(4), 605; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13040605 - 28 Mar 2022
Viewed by 1900
Abstract
Background: The role of genetics in non-steroidal anti-inflammatory drugs (NSAID) exacerbated respiratory disease (NERD) is unclear, with different candidates involved, such as HLA genes, genes related to leukotriene synthesis, and cytokine genes. This study aimed to determine possible associations between 22 polymorphisms in [...] Read more.
Background: The role of genetics in non-steroidal anti-inflammatory drugs (NSAID) exacerbated respiratory disease (NERD) is unclear, with different candidates involved, such as HLA genes, genes related to leukotriene synthesis, and cytokine genes. This study aimed to determine possible associations between 22 polymorphisms in 13 cytokine genes. Methods: We included 195 patients (85 with NERD and 110 with respiratory disease who tolerate NSAIDs) and 156 controls (non-atopic individuals without a history of asthma, nasal polyposis (NP), or NSAID hypersensitivity). Genotyping was performed by sequence-specific primer polymerase chain reaction (PCR-SSP). Amplicons were analyzed by horizontal gel electrophoresis in 2% agarose. Results: Significant differences in allele and genotype frequency distributions were found in TNF (rs1800629), IL4 (rs2243248 and rs2243250), and IL10 (rs1800896, rs1800871, and rs1800872) genes in patients with NSAID hypersensitivity. In all cases, the minor allele and the heterozygous genotype were more prevalent in NERD. An association of TNF rs1800629 SNP with respiratory disease in NSAID-tolerant patients was also found. Conclusions: Retrospectively recorded, we found strong associations of NERD with polymorphisms in IL4, IL10, and TNF genes, suggesting that these genes could be involved in the inflammatory mechanisms underlying NERD. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Allergy Diseases)

Review

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28 pages, 1975 KiB  
Review
The Genetic Factors of the Airway Epithelium Associated with the Pathology of Asthma
by Maral Ranjbar, Christiane E. Whetstone, Hafsa Omer, Lucy Power, Ruth P. Cusack and Gail M. Gauvreau
Genes 2022, 13(10), 1870; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13101870 - 15 Oct 2022
Cited by 10 | Viewed by 3917
Abstract
Asthma is a chronic disease of the airways characterized by inflammation, tightened muscles, and thickened airway walls leading to symptoms such as shortness of breath, chest tightness, and cough in patients. The increased risk of asthma in children of asthmatics parents supports the [...] Read more.
Asthma is a chronic disease of the airways characterized by inflammation, tightened muscles, and thickened airway walls leading to symptoms such as shortness of breath, chest tightness, and cough in patients. The increased risk of asthma in children of asthmatics parents supports the existence of genetic factors involved in the pathogenesis of this disease. Genome-wide association studies have discovered several single nucleotide polymorphisms associated with asthma. These polymorphisms occur within several genes and can contribute to different asthma phenotypes, affect disease severity, and clinical response to different therapies. The complexity in the etiology of asthma also results from interactions between environmental and genetic factors. Environmental exposures have been shown to increase the prevalence of asthma in individuals who are genetically susceptible. This review summarizes what is currently known about the genetics of asthma in relation to risk, response to common treatments, and gene-environmental interactions. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Allergy Diseases)
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18 pages, 1243 KiB  
Review
Genetics and Epigenetics in Allergic Rhinitis
by Bo Yoon Choi, Munsoo Han, Ji Won Kwak and Tae Hoon Kim
Genes 2021, 12(12), 2004; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12122004 - 17 Dec 2021
Cited by 32 | Viewed by 7420
Abstract
The pathogenesis of allergic rhinitis is associated with genetic, environmental, and epigenetic factors. Genotyping of single nucleotide polymorphisms (SNPs) is an advanced technique in the field of molecular genetics that is closely correlated with genome-wide association studies (GWASs) in large population groups with [...] Read more.
The pathogenesis of allergic rhinitis is associated with genetic, environmental, and epigenetic factors. Genotyping of single nucleotide polymorphisms (SNPs) is an advanced technique in the field of molecular genetics that is closely correlated with genome-wide association studies (GWASs) in large population groups with allergic diseases. Many recent studies have paid attention to the role of epigenetics, including alteration of DNA methylation, histone acetylation, and miRNA levels in the pathogenesis of allergic rhinitis. In this review article, genetics and epigenetics of allergic rhinitis, including information regarding functions and significance of previously known and newly-discovered genes, are summarized. Directions for future genetic and epigenetic studies of allergic rhinitis are also proposed. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Allergy Diseases)
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Other

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9 pages, 265 KiB  
Brief Report
C5 and SRGAP3 Polymorphisms Are Linked to Paediatric Allergic Asthma in the Italian Population
by Daria Messelodi, Cristina Giuliani, Francesca Cipriani, Silvia Armuzzi, Emanuela di Palmo, Paolo Garagnani, Luca Bertelli, Annalisa Astolfi, Donata Luiselli, Giampaolo Ricci and Andrea Pession
Genes 2022, 13(2), 214; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13020214 - 25 Jan 2022
Cited by 2 | Viewed by 2109
Abstract
Asthma is a complex and heterogeneous disease, caused by the interaction between genetic and environmental factors with a predominant allergic background in children. The role of specific genes in asthmatic bronchial reactivity is still not clear, probably because of the many common pathways [...] Read more.
Asthma is a complex and heterogeneous disease, caused by the interaction between genetic and environmental factors with a predominant allergic background in children. The role of specific genes in asthmatic bronchial reactivity is still not clear, probably because of the many common pathways shared with other allergic disorders. This study is focused on 11 SNPs possibly related to asthma that were previously identified in a GWAS study. The genetic variability of these SNPs has been analysed in a population of 773 Italian healthy controls, and the presence of an association between the polymorphisms and the asthma onset was evaluated performing genotyping analysis on 108 children affected with asthma compared with the controls. Moreover, a pool of 171 patients with only allergic rhinoconjunctivitis has been included in the case–control analysis. The comparison of allele frequencies in asthmatic patients versus healthy controls identified two SNPs—rs1162394 (p = 0.019) and rs25681 (p = 0.044)—associated with the asthmatic condition, which were not differentially distributed in the rhinoconjunctivitis group. The rs25681 SNP, together with three other SNPs, also resulted in not being homogenously distributed in the Italian population. The significantly higher frequency of the rs25681 and rs1162394 SNPs (located, respectively, in the C5 and SRGAP3 genes) in the asthmatic population suggests an involvement of these genes in the asthmatic context, playing a role in increasing the inflammatory condition that may influence asthma onset and clinical course. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Allergy Diseases)
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