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Molecular Mechanisms of Allergy and Asthma: 3rd Edition
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Molecular Mechanisms of Allergy and Asthma: 3rd Edition

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

Deadline for manuscript submissions: 20 February 2025 | Viewed by 6671

Special Issue Editors

Dr. Bilal Alashkar Alhamwe

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Guest Editor
Institute for Tumor Immunology, Clinic for Hematology, Immunology, and Oncology, Philipps University Marburg, 35043 Marburg, Germany
Interests: allergy; asthma; COPD; epigenetics; gene-environment interactions; lung cancer; microbiome
Special Issues, Collections and Topics in MDPI journals
Dr. Daniel P. Potaczek

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Guest Editor
1. Translational Inflammation Research Division and Core Facility for Single Cell Multiomics, Philipps-University Marburg, 35043 Marburg, Germany
2. Center for Infection and Genomics of the Lung (CIGL), Justus Liebig University of Giessen, 35392 Giessen, Germany
Interests: allergy; asthma; environment; epigenetics; epigenomics; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous successful Special Issues “Molecular Mechanisms of Allergy and Asthma” and “Molecular Mechanisms of Allergy and Asthma 2.0”.

Asthma and other allergic disorders are known to be determined by complex interactions between the individual genetic background and environmental influences. On the molecular level, those are mediated by genetic and epigenetic mechanisms, the latter including DNA methylation, histone modifications, and noncoding regulatory RNAs. Those control expression of immune (regulatory) molecules and this way the function of leukocytes and other types of immune cells involved in the mechanisms underlying the development of allergies. Although our knowledge of the molecular and cellular background of allergic diseases has substantially increased in the last several decades, there is still much to be discovered. Further increase in the understanding of molecular bases of allergic disorders should boost the development of personalized diagnostic and therapeutic approaches. As such, the aims of this Special Issue on “Molecular Mechanisms of Allergy and Asthma 3.0” are to: (1) perform an update (review) on the current status of our knowledge of the contribution of molecular mechanisms to the development and clinical course of asthma and other allergic disorders and (2) further increase this knowledge as well as identify (3) new diagnostic options, and assess their relevance, and (4) molecular targets for novel therapies. Submissions may include original research and different types of reviews.

Dr. Bilal Alashkar Alhamwe
Dr. Daniel P. Potaczek
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • allergy
  • asthma
  • epigenetics/epigenomics
  • genetics/genomics
  • inflammation
  • molecular biology

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Related Special Issues

Published Papers (5 papers)

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Research

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12 pages, 1195 KiB  
Article
Protein Kinase C Isozyme Immaturity/Deficiency in Cord Blood Monocytes and Neutrophils
by Khalida Perveen and Antonio Ferrante
Int. J. Mol. Sci. 2024, 25(21), 11665; https://doi.org/10.3390/ijms252111665 - 30 Oct 2024
Viewed by 453
Abstract
Reduced/deficient expression of Protein Kinase C (PKC)ζ in Cord blood (CB) T cells is associated with allergy development in children and a propensity to maintain an immature T-helper (Th)2 cytokine profile. In addition, other PKC isozymes are also low in CBTCs. Since previous [...] Read more.
Reduced/deficient expression of Protein Kinase C (PKC)ζ in Cord blood (CB) T cells is associated with allergy development in children and a propensity to maintain an immature T-helper (Th)2 cytokine profile. In addition, other PKC isozymes are also low in CBTCs. Since previous studies have reported that cord blood/neonatal monocyte and neutrophil functions are significantly lower than cells from adults, it was of interest to see if the CBTC PKC levels were reflected in CB monocytes and neutrophils. Compared to adult blood, CB expresses low levels of PKCα, β2, ε, θ, μ, ζ and λ/ι in monocytes and PKCα, β2, η, θ, μ, ζ and λ/ι in neutrophils. The T-cell PKCζ levels were positively correlated with levels in CB monocytes but not in neutrophils. However, neither the monocytes nor the neutrophil PKCζ were associated with T-cell development towards a Th1 or Th2 cytokine propensity, based on the production of interferon-gamma and interleukin-4 in response to phytohemagglutinin and phorbol myristate acetate. The results demonstrate that some newborn babies display a deficiency in PKC isozymes in monocytes and neutrophils, as reported for T cells. However, unlike T cells, the PKCζ levels of the phagocytes did not correlate with regulation of development towards a Th1 or Th2 cytokine phenotype. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Allergy and Asthma: 3rd Edition)
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23 pages, 4233 KiB  
Article
Characterization of the Immune-Modulating Properties of Different β-Glucans on Myeloid Dendritic Cells
by Hannah Rainer, Alexandra Goretzki, Yen-Ju Lin, Hannah Ruth Schiller, Maren Krause, Sascha Döring, Daniel Strecker, Ann-Christine Junker, Sonja Wolfheimer, Masako Toda, Stephan Scheurer and Stefan Schülke
Int. J. Mol. Sci. 2024, 25(18), 9914; https://doi.org/10.3390/ijms25189914 - 13 Sep 2024
Viewed by 953
Abstract
In allergen-specific immunotherapy, adjuvants are explored for modulating allergen-specific Th2 immune responses to re-establish clinical tolerance. One promising class of adjuvants are β-glucans, which are naturally derived sugar structures and components of dietary fibers that activate C-type lectin (CLR)-, “Toll”-like receptors (TLRs), and [...] Read more.
In allergen-specific immunotherapy, adjuvants are explored for modulating allergen-specific Th2 immune responses to re-establish clinical tolerance. One promising class of adjuvants are β-glucans, which are naturally derived sugar structures and components of dietary fibers that activate C-type lectin (CLR)-, “Toll”-like receptors (TLRs), and complement receptors (CRs). We characterized the immune-modulating properties of six commercially available β-glucans, using immunological (receptor activation, cytokine secretion, and T cell modulating potential) as well as metabolic parameters (metabolic state) in mouse bone marrow-derived myeloid dendritic cells (mDCs). All tested β-glucans activated the CLR Dectin-1a, whereas TLR2 was predominantly activated by Zymosan. Further, the tested β-glucans differentially induced mDC-derived cytokine secretion and activation of mDC metabolism. Subsequent analyses focusing on Zymosan, Zymosan depleted, β-1,3 glucan, and β-1,3 1,6 glucan revealed robust mDC activation with the upregulation of the cluster of differentiation 40 (CD40), CD80, CD86, and MHCII to different extents. β-glucan-induced cytokine secretion was shown to be, in part, dependent on the activation of the intracellular Dectin-1 adapter molecule Syk. In co-cultures of mDCs with Th2-biased CD4+ T cells isolated from birch allergen Bet v 1 plus aluminum hydroxide (Alum)-sensitized mice, these four β-glucans suppressed allergen-induced IL-5 secretion, while only Zymosan and β-1,3 glucan significantly suppressed allergen-induced interferon gamma (IFNγ) secretion, suggesting the tested β-glucans to have distinct effects on mDC T cell priming capacity. Our experiments indicate that β-glucans have distinct immune-modulating properties, making them interesting adjuvants for future allergy treatment. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Allergy and Asthma: 3rd Edition)
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19 pages, 3502 KiB  
Article
Pulmonary Administration of TLR2/6 Agonist after Allergic Sensitization Inhibits Airway Hyper-Responsiveness and Recruits Natural Killer Cells in Lung Parenchyma
by Justine Devulder, Mathieu Barrier, Julie Carrard, Latiffa Amniai, Coline Plé, Philippe Marquillies, Valérie Ledroit, Bernhard Ryffel, Anne Tsicopoulos, Patricia de Nadai and Catherine Duez
Int. J. Mol. Sci. 2024, 25(17), 9606; https://doi.org/10.3390/ijms25179606 - 4 Sep 2024
Viewed by 1041
Abstract
Asthma is a chronic lung disease with persistent airway inflammation, bronchial hyper-reactivity, mucus overproduction, and airway remodeling. Antagonizing T2 responses by triggering the immune system with microbial components such as Toll-like receptors (TLRs) has been suggested as a therapeutic concept for allergic asthma. [...] Read more.
Asthma is a chronic lung disease with persistent airway inflammation, bronchial hyper-reactivity, mucus overproduction, and airway remodeling. Antagonizing T2 responses by triggering the immune system with microbial components such as Toll-like receptors (TLRs) has been suggested as a therapeutic concept for allergic asthma. The aim of this study was to evaluate the effect of a TLR2/6 agonist, FSL-1 (Pam2CGDPKHPKSF), administered by intranasal instillation after an allergic airway reaction was established in the ovalbumin (OVA) mouse model and to analyze the role of natural killer (NK) cells in this effect. We showed that FSL-1 decreased established OVA-induced airway hyper-responsiveness and eosinophilic inflammation but did not reduce the T2 or T17 response. FSL-1 increased the recruitment and activation of NK cells in the lung parenchyma and modified the repartition of NK cell subsets in lung compartments. Finally, the transfer or depletion of NK cells did not modify airway hyper-responsiveness and eosinophilia after OVA and/or FSL-1 treatment. Thus, the administration of FSL-1 reduces airway hyper-responsiveness and bronchoalveolar lavage eosinophilia. However, despite modifications of their functions following OVA sensitization, NK cells play no role in OVA-induced asthma and its inhibition by FSL-1. Therefore, the significance of NK cell functions and localization in the airways remains to be unraveled in asthma. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Allergy and Asthma: 3rd Edition)
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16 pages, 1982 KiB  
Article
Peripheral Inflammation Featuring Eosinophilia or Neutrophilia Is Associated with the Survival and Infiltration of Eosinophils within the Tumor among Various Histological Subgroups of Patients with NSCLC
by Bilal Alashkar Alhamwe, Kadriya Yuskaeva, Friederike Wulf, Frederik Trinkmann, Mark Kriegsmann, Michael Thomas, Corinna Ulrike Keber, Elke Pogge von Strandmann, Felix J. Herth, Saeed Kolahian, Harald Renz and Thomas Muley
Int. J. Mol. Sci. 2024, 25(17), 9552; https://doi.org/10.3390/ijms25179552 - 3 Sep 2024
Cited by 1 | Viewed by 1471
Abstract
Immune activation status determines non-small cell lung cancer (NSCLC) prognosis, with reported positive/negative associations for T helper type 2 (TH2) responses, including allergen-specific IgE and eosinophils. Our study seeks to explore the potential impact of these comorbid immune responses on the survival rates [...] Read more.
Immune activation status determines non-small cell lung cancer (NSCLC) prognosis, with reported positive/negative associations for T helper type 2 (TH2) responses, including allergen-specific IgE and eosinophils. Our study seeks to explore the potential impact of these comorbid immune responses on the survival rates of patients with NSCLC. Our retrospective study used data from the Data Warehouse of the German Center for Lung Research (DZL) and Lung Biobank at Thoraxklinik Heidelberg. We estimated the association of blood eosinophilia and neutrophilia on survival rates in an inflammatory cohort of 3143 patients with NSCLC. We also tested sensitization to food and inhalants and high-sensitivity C-reactive protein (hs-CRP) in a comorbidity cohort of 212 patients with NSCLC. Finally, we estimated the infiltration of immune-relevant cells including eosinophils, T-cells, and mast cells in a tissue inflammatory sub-cohort of 60 patients with NSCLC. Sensitization to at least one food or inhalant (sIgE) was higher in patients with adenocarcinoma (adeno-LC) than the non-adenocarcinoma (non-adeno-LC). Furthermore, hs-CRP was higher in non-adeno-LC compared with adeno-LC. Peripheral inflammation, particularly eosinophilia and neutrophilia, was associated with poor survival outcomes in NSCLC with a clear difference between histological subgroups. Finally, blood eosinophilia was paralleled by significant eosinophil infiltration into the peritumoral tissue in the lung. This study provides novel perspectives on the crucial role of peripheral inflammation, featuring eosinophilia and neutrophilia, with overall survival, underscoring distinctions between NSCLC subgroups (adeno-LC vs. non-adeno-LC). Peripheral eosinophilia enhances eosinophil infiltration into tumors. This sheds light on the complex interplay between inflammation, eosinophil infiltration, and NSCLC prognosis among various histological subtypes. Further studies are required to underscore the role of eosinophils in NSCLC among different histological subgroups and their role in shaping the tumor microenvironment. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Allergy and Asthma: 3rd Edition)
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Review

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18 pages, 2298 KiB  
Review
Prenatal Factors in the Development of Allergic Diseases
by Manuela Grijincu, Maria-Roxana Buzan, Lauriana-Eunice Zbîrcea, Virgil Păunescu and Carmen Panaitescu
Int. J. Mol. Sci. 2024, 25(12), 6359; https://doi.org/10.3390/ijms25126359 - 8 Jun 2024
Cited by 1 | Viewed by 1944
Abstract
Allergic diseases are showing increasing prevalence in Western societies. They are characterized by a heightened reactivity towards otherwise harmless environmental stimuli. Allergic diseases showing a wide range of severity of symptoms have a significant impact on the quality of life of affected individuals. [...] Read more.
Allergic diseases are showing increasing prevalence in Western societies. They are characterized by a heightened reactivity towards otherwise harmless environmental stimuli. Allergic diseases showing a wide range of severity of symptoms have a significant impact on the quality of life of affected individuals. This study aims to highlight the mechanisms that induce these reactions, how they progress, and which prenatal factors influence their development. Most frequently, the reaction is mediated by immunoglobulin E (IgE) produced by B cells, which binds to the surface of mast cells and basophils and triggers an inflammatory response. The antibody response is triggered by a shift in T-cell immune response. The symptoms often start in early childhood with eczema or atopic dermatitis and progress to allergic asthma in adolescence. An important determinant of allergic diseases seems to be parental, especially maternal history of allergy. Around 30% of children of allergic mothers develop allergic sensitization in childhood. Genes involved in the regulation of the epithelial barrier function and the T-cell response were found to affect the predisposition to developing allergic disorders. Cord blood IgE was found to be a promising predictor of allergic disease development. Fetal B cells produce IgE starting at the 20th gestation week. These fetal B cells could be sensitized together with mast cells by maternal IgE and IgE–allergen complexes crossing the placental barrier via the low-affinity IgE receptor. Various factors were found to facilitate these sensitizations, including pesticides, drugs, exposure to cigarette smoke and maternal uncontrolled asthma. Prenatal exposure to microbial infections and maternal IgG appeared to play a role in the regulation of T-cell response, indicating a protective effect against allergy development. Additional preventive factors were dietary intake of vitamin D and omega 3 fatty acids as well as decreased maternal IgE levels. The effect of exposure to food allergens during pregnancy was inconclusive, with studies having found both sensitizing and protective effects. In conclusion, prenatal factors including genetics, epigenetics and fetal environmental factors have an important role in the development of allergic disorders in later life. Children with a genetic predisposition are at risk when exposed to cigarette smoke as well as increased maternal IgE in the prenatal period. Maternal diet during pregnancy and immunization against certain allergens could help in the prevention of allergy in predisposed children. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Allergy and Asthma: 3rd Edition)
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