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Special Issue "Allergic Airway Disease: Molecular Immunology, Pathogenesis and Inflammation 2.0"

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: closed (28 February 2021).

Special Issue Editors

Prof. Dr. Hiroaki Kume
E-Mail Website
Guest Editor
Department of Respiratory Medicine and Allergology, Faculty of Medicine, Kindai University, Osakasayama 589-8511, Japan
Interests: respiratory medicine; allergy and pharmacology; β2-aderenergic agonists; muscarinic receptor antagonists; airway smooth muscle
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Yoshihiko Chiba
E-Mail Website
Guest Editor
Laboratory of Molecular Biology and Physiology, Hoshi University, Tokyo, Japan
Interests: allergic bronchial asthma; airway hyperresponsiveness; smooth muscle; allergic rhinitis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announced the continuation of our Special Issue “Allergic Airway Disease: Molecular Immunology, Pathogenesis, and Inflammation” with a second edition.

Asthma and related respiratory tract allergic diseases (allergic rhinitis, sinusitis) are among the most common chronic diseases in adults and children. However, the disease course is still difficult to be predicted, and the treatment remains nonspecific and potentially hazardous. Allergic airway diseases are characterized by T-helper type 2 (Th2)-skewed eosinophilic inflammation, mucus hypersecretion, as well as airway hyperresponsiveness. In addition, in the initiation and development of allergic airway disease, excessive activation of Th2 cells due to insufficient suppression of regulatory T cells (Tregs) is thought to play a key role. An improved understanding of the fundamental factors that initiate allergic inflammation, especially Th2 cell induction, may lead to an improved clinical management of these diseases. Human monoclonal antibodies against IgE and IL-5 have been used clinically; however, there are still many problems in advancing therapy towards a cure for these diseases. Not only scientific but also clinical approaches are needed to achieve this objective.

This Special Issue will focus on, but not be limited to, recent advances across the developmental spectrum on the mechanisms underlying allergic airways diseases, including molecular immunology, pathogenesis, inflammation, and the role of genetic and environmental factors.

Prof. Dr. Hiroaki Kume
Prof. Dr. Yoshihiko Chiba
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 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. 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

  • Asthma
  • Allergic airway disease (allergic rhinitis, sinusitis)
  • Airway smooth muscle
  • Airway hyperresponsiveness
  • Eosinophil inflammation
  • Mast cells
  • Cytokines
  • Ca2+ signaling
  • Mucus hypersecretion
  • Ion channel
  • Airway eosinophilia
  • Immune
  • IgE
  • Genetic
  • Environmental factors

Related Special Issue

Published Papers (3 papers)

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Research

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Article
Downregulation of miR-140-3p Contributes to Upregulation of CD38 Protein in Bronchial Smooth Muscle Cells
Int. J. Mol. Sci. 2020, 21(21), 7982; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21217982 - 27 Oct 2020
Cited by 1 | Viewed by 669
Abstract
In allergic bronchial asthma, an increased smooth muscle contractility of the airways is one of the causes of the airway hyperresponsiveness (AHR). Increasing evidence also suggests a possible involvement of microRNAs (miRNAs) in airway diseases, including asthma, although their roles in function and [...] Read more.
In allergic bronchial asthma, an increased smooth muscle contractility of the airways is one of the causes of the airway hyperresponsiveness (AHR). Increasing evidence also suggests a possible involvement of microRNAs (miRNAs) in airway diseases, including asthma, although their roles in function and pathology largely unknown. The current study aimed to determine the role of a miRNA, miR-140-3p, in the control of protein expression of CD38, which is believed to regulate the contraction of smooth muscles, including the airways. In bronchial smooth muscles (BSMs) of the mice that were actively sensitized and repeatedly challenged with ovalbumin antigen, an upregulation of CD38 protein concurrently with a significant reduction of miR-140-3p was observed. In cultured human BSM cells (hBSMCs), transfection with a synthetic miR-140-3p inhibitor caused an increase in CD38 protein, indicating that its basal protein expression is regulated by endogenous miR-140-3p. Treatment of the hBSMCs with interleukin-13 (IL-13), an asthma-related cytokine, caused both an upregulation of CD38 protein and a downregulation of miR-140-3p. Transfection of the hBSMCs with miR-140-3p mimic inhibited the CD38 protein upregulation induced by IL-13. On the other hand, neither a CD38 product cyclic ADP-ribose (cADPR) nor its antagonist 8-bromo-cADPR had an effect on the BSM contraction even in the antigen-challenged mice. Taken together, the current findings suggest that the downregulation of miR-140-3p induced by IL-13 might cause an upregulation of CD38 protein in BSM cells of the disease, although functional and pathological roles of the upregulated CD38 are still unclear. Full article
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Article
Acid Stripping of Surface IgE Antibodies Bound to FcεRI Is Unsuitable for the Functional Assays That Require Long-Term Culture of Basophils and Entire Removal of Surface IgE
Int. J. Mol. Sci. 2020, 21(2), 510; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21020510 - 13 Jan 2020
Cited by 2 | Viewed by 1290
Abstract
Basophils are rare granulocytes and dysregulated functions of these cells are associated with several atopic and non-atopic allergic diseases of skin, respiratory system and gastrointestinal tract. Both cytokines and immunoglobulin E (IgE) are implicated in mediating the basophil activation and pathogenesis of these [...] Read more.
Basophils are rare granulocytes and dysregulated functions of these cells are associated with several atopic and non-atopic allergic diseases of skin, respiratory system and gastrointestinal tract. Both cytokines and immunoglobulin E (IgE) are implicated in mediating the basophil activation and pathogenesis of these disorders. Several reports have shown that healthy individuals, and patients with allergic disorders display IgG autoantibodies to IgE and hence functional characterization of these anti-IgE IgG autoantibodies is critical. In general, anti-IgE IgG autoantibodies modulate basophil activation irrespective of allergen specificity by interacting with constant domains of IgE. Therefore, an ideal solution to prove the functions of such anti-IgE IgG autoantibodies would be to completely eliminate type I high affinity immunoglobulin E receptor (FcɛRI)-bound IgE from the surface of basophils and to demonstrate in an unequivocal manner the role of anti-IgE IgG autoantibodies. In line with previous reports, our data show that FcɛRI on peripheral blood basophils are almost saturated with IgE. Further, acetic acid buffer (pH 4) efficiently removes these FcɛRI-bound IgE. Although immediately following acetic acid-elution of IgE had no repercussion on the viability of basophils, following 24 h culture with interleukin-3 (IL-3), the viability and yield of basophils were drastically reduced in acid-treated cells and had repercussion on the induction of activation markers. Lactic acid treatment on the other hand though had no adverse effects on the viability of basophils and IL-3-induced activation, it removed only a small fraction of the cell surface bound IgE. Thus, our results show that acid buffers could be used for the elution of FcɛRI-bound IgE on the basophil surface for the biochemical characterization of IgE antibodies or for the immediate use of basophils to determine their sensitivity to undergo degranulation by specific allergens. However, these methods are not utile for the functional assays of basophils that require longer duration of culture and entire removal of surface IgE to validate the role of anti-IgE IgG autoantibodies that interact with FcɛRI-bound IgE irrespective of allergen specificity. Full article
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Review

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Review
Role of CD4+ T Cells in Allergic Airway Diseases: Learning from Murine Models
Int. J. Mol. Sci. 2020, 21(20), 7480; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207480 - 11 Oct 2020
Cited by 3 | Viewed by 739
Abstract
The essential contribution of CD4+ T cells in allergic airway diseases has been demonstrated, especially by using various murine models of antigen-induced airway inflammation. In addition to antigen-immunized mouse models employing mast cell-deficient mice and CD4+ T cell-depleting procedure, antigen-specific CD4 [...] Read more.
The essential contribution of CD4+ T cells in allergic airway diseases has been demonstrated, especially by using various murine models of antigen-induced airway inflammation. In addition to antigen-immunized mouse models employing mast cell-deficient mice and CD4+ T cell-depleting procedure, antigen-specific CD4+ T cell transfer models have revealed the possible development of allergic inflammation solely dependent on CD4+ T cells. Regardless of the classical Th1/Th2 theory, various helper T cell subsets have the potential to induce different types of allergic inflammation. T cell receptor (TCR)-transgenic (Tg) mice have been used for investigating T cell-mediated immune responses. Besides, we have recently generated cloned mice from antigen-specific CD4+ T cells through somatic cell nuclear transfer. In contrast to TCR-Tg mice that express artificially introduced TCR, the cloned mice express endogenously regulated antigen-specific TCR. Upon antigen exposure, the mite antigen-reactive T cell-cloned mice displayed strong airway inflammation accompanied by bronchial hyperresponsiveness in a short time period. Antigen-specific CD4+ T cell-cloned mice are expected to be useful for investigating the detailed role of CD4+ T cells in various allergic diseases and for evaluating novel anti-allergic drugs. Full article
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