Special Issue "The Molecular and Cellular Basis for Allergies & Asthma"

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 15 August 2019

Special Issue Editor

Guest Editor
Prof. Dr. Cenk Suphioglu

School of Life and Environmental Sciences, Faculty of Science, Engineering and Built Environment, Deakin University, Waurn Ponds, Victoria 3216, Australia
Website 1 | Website 2 | E-Mail
Interests: allergy; allergens; pollen allergens; peanut allergens; egg allergens; thunderstorm asthma; allergic asthma; recombinant allergens; aerobiology; allergy diagnostics; allergy therapeutics; beta secretase; BACE1; neuronal cells; neurodegeneration; Alzheimer’s disease

Special Issue Information

Dear Colleagues,

Welcome to this Special Issue of Cells on “Molecular and Cellular Basis for Allergies and Asthma"

Allergies and Asthma are chronic health conditions that range in frequency and severity from mild to life-threatening symptoms, which vary from person to person. In particular, the importance of allergic asthma gained much international press and attention following Melbourne’s recent deadly thunderstorm asthma epidemic of November 21, 2016, which resulted in 10 deaths and thousands of sufferers seeking emergency medical attention. Although one can suffer from allergies without ever having a previous episode of an asthma attack, it is now known and well accepted that people with certain allergies (grass pollen and fungal spore allergies for example) can be particularly vulnerable to thunderstorm asthma epidemics and thus the importance of research on the molecular and cellular basis for allergies and asthma.

This Special Issue is intended to present latest findings related to the molecular and cellular basis for allergies and asthma, as well as the molecular and cellular links between the two conditions. Original research and review articles on all topics related to molecular and cellular basis for allergies and asthma are invited. I have the pleasure in inviting research scientists and clinicians from all relevant fields to submit their papers for this important and timely Special Issue. Please accept my sincere thanks for choosing to publish in Cells and I look forward to your submissions for this highly interesting, relevant and important Special Issue.

Assoc. Prof. Cenk Suphioglu
Guest Editor

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 papers will be 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. Cells 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 1800 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

  • Allergens
  • Allergic Asthma
  • Allergic rhinitis
  • Allergy
  • Asthma
  • Atopy
  • B cells
  • Basophils
  • Cellular Allergy
  • Cellular Asthma
  • Dendritic cells
  • Eosinophils
  • Helper T cells
  • Hypersensitivity
  • IgE
  • IL-4
  • IL-5
  • IL-13
  • Mast cells
  • Molecular Allergy
  • Molecular Asthma
  • Regulatory T cells
  • STAT6
  • Th1 cells
  • Th2 cells
  • Thunderstorm Asthma

Published Papers (3 papers)

View options order results:
result details:
Displaying articles 1-3
Export citation of selected articles as:

Research

Jump to: Review

Open AccessArticle
NFκB- and MAP-Kinase Signaling Contribute to the Activation of Murine Myeloid Dendritic Cells by a Flagellin A: Allergen Fusion Protein
Received: 12 December 2018 / Revised: 26 March 2019 / Accepted: 12 April 2019 / Published: 15 April 2019
PDF Full-text (3079 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Fusion proteins incorporating the TLR5-ligand flagellin are currently undergoing clinical trials as vaccine candidates for many diseases. We recently reported a flagellin:allergen fusion protein containing the TLR5-ligand flagellin A (FlaA) from Listeria monocytogenes and the major birch pollen allergen Bet v 1 (rFlaA:Betv1) [...] Read more.
Fusion proteins incorporating the TLR5-ligand flagellin are currently undergoing clinical trials as vaccine candidates for many diseases. We recently reported a flagellin:allergen fusion protein containing the TLR5-ligand flagellin A (FlaA) from Listeria monocytogenes and the major birch pollen allergen Bet v 1 (rFlaA:Betv1) to prevent allergic sensitization in an experimental mouse model. This study analyzes the signaling pathways contributing to rFlaA:Betv1-mediated pro- and anti-inflammatory cytokine secretion and cell metabolism in myeloid dendritic cells (mDCs) in vitro. The influence of mammalian target of rapamycin (mTOR)-, NFκB-, and MAP kinase (MAPK)-signaling on cytokine secretion and metabolic activity of bone marrow (BM)-derived mDCs stimulated with rFlaA:Betv1 were investigated by pre-treatment with either mTOR- (rapamycin), NFκB- (dexamethason, BMS-345541, TPCA-1, triptolide, or BAY-11) or MAPK- (SP600125, U0126, or SB202190) inhibitors, respectively. rFlaA:Betv1-mediated IL-10 secretion as well as activation of mDC metabolism, rather than pro-inflammatory cytokine secretion, were inhibited by rapamycin. Inhibition of NFκB-signaling suppressed rFlaA:Betv1-induced IL-12, while inhibition of MAPK-signaling dose-dependently suppressed rFlaA:Betv1-induced IL-10 as well as pro-inflammatory IL-6 and TNF-α production. Notably, with the exception of a partial JNK-dependency, rFlaA:Betv1-mediated effects on mDC metabolism were mostly NFκB- and MAPK-independent. Therefore, MAPK-mediated activation of both NFκB- and mTOR-signaling likely is a key pathway for the production of pro- and anti-inflammatory cytokines by flagellin fusion protein vaccines. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Allergies & Asthma)
Figures

Figure 1

Review

Jump to: Research

Open AccessReview
Mouse Models for Food Allergies: Where Do We Stand?
Received: 14 May 2019 / Revised: 31 May 2019 / Accepted: 4 June 2019 / Published: 6 June 2019
PDF Full-text (3274 KB) | HTML Full-text | XML Full-text
Abstract
Food allergies are a steadily increasing health and economic problem. Immunologically, food allergic reactions are caused by pathological, allergen-specific Th2 responses resulting in IgE-mediated mast cell degranulation and associated inflammatory reactions. Clinically, food allergies are characterized by local inflammation of the mouth mucosa, [...] Read more.
Food allergies are a steadily increasing health and economic problem. Immunologically, food allergic reactions are caused by pathological, allergen-specific Th2 responses resulting in IgE-mediated mast cell degranulation and associated inflammatory reactions. Clinically, food allergies are characterized by local inflammation of the mouth mucosa, the face, the throat, the gastrointestinal tract, are frequently paralleled by skin reactions, and can result in life-threatening anaphylactic reactions. To better understand food allergies and establish novel treatment options, mouse models are indispensable. This review discusses the available mouse food allergy models, dividing them into four categories: (1) adjuvant-free mouse models, (2) mouse models relying on adjuvants to establish allergen-specific Th2 responses, (3) mouse models using genetically-modified mouse strains to allow for easier sensitization, and (4) humanized mouse models in which different immunodeficient mouse strains are reconstituted with human immune or stem cells to investigate humanized immune responses. While most of the available mouse models can reproducibly portray the immunological parameters of food allergy (Th2 immune responses, IgE production and mast cell activation/expansion), so far, the recreation of the clinical parameters has proven more difficult. Therefore, up to now none of the available mouse models can reproduce the complete human pathology. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Allergies & Asthma)
Figures

Figure 1

Open AccessReview
A Review of Macrophage MicroRNAs’ Role in Human Asthma
Received: 1 April 2019 / Revised: 1 May 2019 / Accepted: 7 May 2019 / Published: 8 May 2019
PDF Full-text (851 KB) | HTML Full-text | XML Full-text
Abstract
There is an imbalance in asthma between classically activated macrophages (M1 cells) and alternatively activated macrophages (M2 cells) in favor of the latter. MicroRNAs (miRNAs) play a critical role in regulating macrophage proliferation and differentiation and control the balance of M1 and M2 [...] Read more.
There is an imbalance in asthma between classically activated macrophages (M1 cells) and alternatively activated macrophages (M2 cells) in favor of the latter. MicroRNAs (miRNAs) play a critical role in regulating macrophage proliferation and differentiation and control the balance of M1 and M2 macrophage polarization, thereby controlling immune responses. Here we review the current published data concerning miRNAs with known correlation to a specific human macrophage phenotype and polarization, and their association with adult asthma. MiRNA-targeted therapy is still in the initial stages, but clinical trials are under recruitment or currently running for some miRNAs in other diseases. Regulating miRNA expression via their upregulation or downregulation could show potential as a novel therapy for improving treatment efficacy in asthma. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Allergies & Asthma)
Figures

Figure 1

Cells EISSN 2073-4409 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top