Special Issue "Eosinophilic Inflammation"

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: 31 December 2020.

Special Issue Editors

Dr. Akira Kanda
Website
Guest Editor
Kansai Medical University, Department of Otorhinolaryngology, Moriguchi, Japan
Interests: airway inflammation; allergic rhinitis; asthma; eosinophil; sinusitis; united airway
Dr. David Dombrowicz
Website
Guest Editor
EGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, University of Lille, 59019 Lille, France
Interests: allergy; inflammation; cardiac & cardiovascular systems

Special Issue Information

Dear colleagues,

The focus of this Special Issue is eosinophilic inflammation such as allergic rhinitis, asthma, chronic rhinosinusitis with nasal polyp, esophagitis, gastroenteritis, and otitis media.

Eosinophils are key contributors to Th2-associated pathologies such as allergic disorders. They also function as effectors in the innate immune response through the expression of Toll-like receptors. In the inflamed site, activated eosinophils exert their effects through cytotoxic mediators, comprising granules (EPO, MBP, ECP, and EDN), cytokines, chemokines, and lipid mediators, resulting in tissue damage. However, little is known about the mechanisms of pathogenesis by activated eosinophils.  

Here, we focus not only all clinical investigations involved in eosinophils-derived disorders but also basic on investigations in vitro and in vivo using animal models.   

Dr. Akira Kanda
Dr. David Dombrowicz
Guest Editors

Manuscript Submission Information

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Keywords

  • airway inflammation
  • allergic rhinitis
  • asthma
  • chronic rhinosinusitis with nasal polyp
  • eosinophil
  • esophagitis
  • gastroenteritis
  • otitis media
  • united airway disease
  • atopic dermatitis
  • airway hyperresponsiveness (AHR)

Published Papers (3 papers)

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Research

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Open AccessArticle
Reduced Local Response to Corticosteroids in Eosinophilic Chronic Rhinosinusitis with Asthma
Biomolecules 2020, 10(2), 326; https://doi.org/10.3390/biom10020326 - 18 Feb 2020
Cited by 1
Abstract
Eosinophilic chronic rhinosinusitis (ECRS), a subgroup of chronic rhinosinusitis with nasal polyps, is recognized as a refractory eosinophilic disorder characterized by both upper and lower airway inflammation. In some severe cases, disease control is poor, likely due to local steroid insensitivity. In this [...] Read more.
Eosinophilic chronic rhinosinusitis (ECRS), a subgroup of chronic rhinosinusitis with nasal polyps, is recognized as a refractory eosinophilic disorder characterized by both upper and lower airway inflammation. In some severe cases, disease control is poor, likely due to local steroid insensitivity. In this study, we focused on protein phosphatase 2A (PP2A), a key factor regulating glucocorticoid receptor (GR) nuclear translocation, and examined its association with local responses to corticosteroids in eosinophilic airway inflammation. Our results indicated reduced responses to corticosteroids in nasal epithelial cells from ECRS patients with asthma, which were also associated with decreased PP2A mRNA expression. Eosinophil peroxidase stimulates elevated PP2A phosphorylation levels, reducing PP2A protein expression and activity. In addition, mRNA levels of inflammatory mediators (TSLP, IL-25, IL-33, CCL4, CCL5, CCL11, and CCL26) associated with eosinophilic airway inflammation in epithelial cells were increased in nasal polyps (eosinophil-rich areas) compared with those in uncinate process tissues (eosinophil-poor areas) from the same patients. PP2A reduction by siRNA reduced GR nuclear translocation, whereas PP2A overexpression by plasmid transfection, or PP2A activation by formoterol, enhanced GR nuclear translocation. Collectively, our findings indicate that PP2A may represent a promising therapeutic target in refractory eosinophilic airway inflammation characterized by local steroid insensitivity. Full article
(This article belongs to the Special Issue Eosinophilic Inflammation)
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Open AccessArticle
A Novel Approach for Investigating Upper Airway Hyperresponsiveness Using Micro-CT in Eosinophilic Upper Airway Inflammation such as Allergic Rhinitis Model
Biomolecules 2019, 9(7), 252; https://doi.org/10.3390/biom9070252 - 27 Jun 2019
Abstract
Airway hyperresponsiveness (AHR) has been proposed as a feature of pathogenesis of eosinophilic upper airway inflammation such as allergic rhinitis (AR). The measurement system for upper AHR (UAHR) in rodents is poorly developed, although measurements of nasal resistance have been reported. [...] Read more.
Airway hyperresponsiveness (AHR) has been proposed as a feature of pathogenesis of eosinophilic upper airway inflammation such as allergic rhinitis (AR). The measurement system for upper AHR (UAHR) in rodents is poorly developed, although measurements of nasal resistance have been reported. Here we assessed UAHR by direct measurement of swelling of the nasal mucosa induced by intranasal methacholine (MCh) using micro-computed tomography (micro-CT). Micro-CT analysis was performed in both naïve and ovalbumin-induced AR mice following intranasal administration of MCh. The nasal cavity was segmented into two-dimensional horizontal and axial planes, and the data for nasal mucosa were acquired for the region of interest threshold. Then, a ratio between the nasal mucosa area and nasal cavity area was calculated as nasal mucosa index. Using our novel method, nasal cavity structure was clearly identified on micro-CT, and dose-dependent increased swelling of the nasal mucosa was observed upon MCh treatment. Moreover, the nasal mucosa index was significantly increased in AR mice compared to controls following MCh treatment, while ovalbumin administration did not affect swelling of the nasal mucosa in either group. This UAHR following MCh treatment was completely reversed by pretreatment with glucocorticoids. This novel approach using micro-CT for investigating UAHR reflects a precise assessment system for swelling of the nasal mucosa following MCh treatment; it not only sheds light on the mechanism of AR but also contributes to the development of new therapeutic drugs in AR patients. Full article
(This article belongs to the Special Issue Eosinophilic Inflammation)
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Review

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Open AccessReview
Possible Mechanisms of Eosinophil Accumulation in Eosinophilic Pneumonia
Biomolecules 2020, 10(4), 638; https://doi.org/10.3390/biom10040638 - 21 Apr 2020
Abstract
Eosinophilic pneumonia (EP), including acute EP and chronic EP, is characterized by the massive pulmonary infiltration of eosinophils into the lung. However, the mechanisms underlying the selective accumulation of eosinophils in EP have not yet been fully elucidated. We reported that bronchoalveolar lavage [...] Read more.
Eosinophilic pneumonia (EP), including acute EP and chronic EP, is characterized by the massive pulmonary infiltration of eosinophils into the lung. However, the mechanisms underlying the selective accumulation of eosinophils in EP have not yet been fully elucidated. We reported that bronchoalveolar lavage fluid (BALF) from EP patients induced the transmigration of eosinophils across endothelial cells in vitro. The concentrations of eotaxin-2 (CCL24) and monocyte chemotactic protein (MCP)-4 (CCL13), which are CC chemokine receptor (CCR) 3 ligands, were elevated in the BALF of EP patients, and anti-CCR3 monoclonal antibody inhibited the eosinophil transmigration induced by the BALF of EP patients. The concentration of macrophage inflammatory protein 1β (CCL4), a CCR5 ligand that induces eosinophil migration, was increased in the BALF of EP patients. Furthermore, the concentration of interleukin (IL) 5 was increased in the BALF of EP patients, and it has been reported that anti-IL-5 antibody treatment resulted in remission and the reduction of glucocorticoid use in some cases of chronic EP. The concentrations of lipid mediators, such as leukotriene (LT) B4, damage-associated molecular pattern molecules (DAMPs), such as uric acid, or extracellular matrix proteins, such as periostin, were also increased in the BALF of EP patients. These findings suggest that chemokines, such as CCR3/CCR5 ligands, cytokines, such as IL-5, lipid mediators, such as LTB4, DAMPs, and extracellular matrix proteins may play roles in the accumulation or activation of eosinophils in EP. Full article
(This article belongs to the Special Issue Eosinophilic Inflammation)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

1. Title: "Possible mechanism of eosinophil accumulation into the airway in eosinophilic pneumonia"
Authors: Kazuyuki Nakagome et al.

2. Authors: David Dombrowicz et al.

3. Authors: Fanny Legrand et al.

4. Authors: Kobayashi Yoshiki et al.

5. Title: "Multiple food elimination diet as a steroid sparing treatment for eosinophilic gastroenteritis: a case report and literature review of efficacy of dietary treatment for eosinophilic gastroenteritis". Authors: Yoshiyuki Yamada et al.

6. Authors: Delphine Staumont et al.

7. Authors: V.D. Bui et al.

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