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Novel Insights into Molecular Mechanisms and Therapy of Asthma
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Novel Insights into Molecular Mechanisms and Therapy of Asthma

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 15 February 2025 | Viewed by 12665

Special Issue Editor

Dr. Marco Caminati

E-Mail Website
Guest Editor
Asthma Center and Allergy Unit, Center for Hypereosinophilic Dysimmune Conditions, University of Verona, Verona University Hospital, 37126 Verona, Italy
Interests: allergy and clinical immunology; severe asthma; immunoterapy; biologic drugs; hyperesoinophilic dysimmune conditions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The overall knowledge about asthma pathobiology has increased considerably in recent years. Novel insights from genetics and epigenetics as regards tissue and humoral inflammation drivers have contributed to better clarify the mechanism underlying the clinical expressions of bronchial asthma, as well as its different endotypes and phenotypes.  Furthermore, new experimental and clinical evidence has paved the way for the development of targeted therapies by selectively addressing the major players in asthma pathobiology, including eosinophils, T2 cytokines and alarmins.

However, some issues still limit a full precision medicine approach to asthma patients. Easily available biomarkers, including blood eosinophils, serum IgE and exhaled nitric oxide (FeNO), although quite informative about the wide spectrum of T2 high inflammation, are not accurate enough to unequivocally define asthma phenotypes or the major molecular driver leading the immune cascade at the moment we evaluate our patients. The “translational gap” between the immunological features of the asthma pathobiological background and the possibility of accurately identifying their clinical counterpart always impacts the treatment selection process. In fact, the identification of the best responder patient to each targeted therapy might be hampered by the poor accuracy of the clinical biomarkers we currently have.

This Special Issue of Cells will address both experimental and translational evidence as well as high-quality data that may contribute to fill the gap.

Dr. Marco Caminati
Guest Editor

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Published Papers (4 papers)

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Research

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12 pages, 2729 KiB  
Article
The Neutralization of the Eosinophil Peroxidase Antibody Accelerates Eosinophilic Mucin Decomposition
by Yoshiki Kobayashi, Hanh Hong Chu, Dan Van Bui, Yasutaka Yun, Linh Manh Nguyen, Akitoshi Mitani, Kensuke Suzuki, Mikiya Asako, Akira Kanda and Hiroshi Iwai
Cells 2023, 12(23), 2746; https://doi.org/10.3390/cells12232746 - 30 Nov 2023
Cited by 1 | Viewed by 1240
Abstract
Eosinophilic airway inflammation, complicated by bronchial asthma and eosinophilic chronic rhinosinusitis (ECRS), is difficult to treat. The disease may become refractory when eosinophilic mucin associated with eosinophil peroxidase (EPX) and autoantibodies fills in the paranasal sinus and small airway. This study investigated the [...] Read more.
Eosinophilic airway inflammation, complicated by bronchial asthma and eosinophilic chronic rhinosinusitis (ECRS), is difficult to treat. The disease may become refractory when eosinophilic mucin associated with eosinophil peroxidase (EPX) and autoantibodies fills in the paranasal sinus and small airway. This study investigated the functional role of an anti-EPX antibody in eosinophilic mucin of ECRS in eosinophilic airway inflammation. Eosinophilic mucin was obtained from patients with ECRS. The effects of the anti-EPX antibody on dsDNA release from eosinophils and eosinophilic mucin decomposition were evaluated. Immunofluorescence or enzyme-linked immunosorbent assays were performed to detect the anti-EPX antibody and its supernatant and serum levels in eosinophilic mucin, respectively. The serum levels of the anti-EPX antibody were positively correlated with sinus computed tomography score and fractionated exhaled nitrogen oxide. Patients with refractory ECRS had higher serum levels of the anti-EPX antibody than those without. However, dupilumab treatment decreased the serum levels of the anti-EPX antibody. Immunoglobulins (Igs) in the immunoprecipitate of mucin supernatants enhanced dsDNA release from eosinophils, whereas the neutralization of Igs against EPX stopped dsDNA release. Furthermore, EPX antibody neutralization accelerated mucin decomposition and restored corticosteroid sensitivity. Taken together, the anti-EPX antibody may be involved in the formulation of eosinophilic mucin and be used as a clinical marker and therapeutic target for intractable eosinophilic airway inflammation. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms and Therapy of Asthma)
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Review

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23 pages, 1998 KiB  
Review
The Role of Transforming Growth Factor-β (TGF-β) in Asthma and Chronic Obstructive Pulmonary Disease (COPD)
by Krzysztof Kraik, Maciej Tota, Julia Laska, Julia Łacwik, Łukasz Paździerz, Łukasz Sędek and Krzysztof Gomułka
Cells 2024, 13(15), 1271; https://doi.org/10.3390/cells13151271 - 29 Jul 2024
Viewed by 1009
Abstract
Asthma and chronic obstructive pulmonary disease (COPD) represent chronic inflammatory respiratory disorders that, despite having distinct pathophysiological underpinnings, both feature airflow obstruction and respiratory symptoms. A critical component in the pathogenesis of each condition is the transforming growth factor-β (TGF-β), a multifunctional cytokine [...] Read more.
Asthma and chronic obstructive pulmonary disease (COPD) represent chronic inflammatory respiratory disorders that, despite having distinct pathophysiological underpinnings, both feature airflow obstruction and respiratory symptoms. A critical component in the pathogenesis of each condition is the transforming growth factor-β (TGF-β), a multifunctional cytokine that exerts varying influences across these diseases. In asthma, TGF-β is significantly involved in airway remodeling, a key aspect marked by subepithelial fibrosis, hypertrophy of the smooth muscle, enhanced mucus production, and suppression of emphysema development. The cytokine facilitates collagen deposition and the proliferation of fibroblasts, which are crucial in the structural modifications within the airways. In contrast, the role of TGF-β in COPD is more ambiguous. It initially acts as a protective agent, fostering tissue repair and curbing inflammation. However, prolonged exposure to environmental factors such as cigarette smoke causes TGF-β signaling malfunction. Such dysregulation leads to abnormal tissue remodeling, marked by excessive collagen deposition, enlargement of airspaces, and, thus, accelerated development of emphysema. Additionally, TGF-β facilitates the epithelial-to-mesenchymal transition (EMT), a process contributing to the phenotypic alterations observed in COPD. A thorough comprehension of the multifaceted role of TGF-β in asthma and COPD is imperative for elaborating precise therapeutic interventions. We review several promising approaches that alter TGF-β signaling. Nevertheless, additional studies are essential to delineate further the specific mechanisms of TGF-β dysregulation and its potential therapeutic impacts in these chronic respiratory diseases. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms and Therapy of Asthma)
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31 pages, 1689 KiB  
Review
Eosinophilic Asthma: Pathophysiology and Therapeutic Horizons
by Musaddique Hussain and Gang Liu
Cells 2024, 13(5), 384; https://doi.org/10.3390/cells13050384 - 23 Feb 2024
Cited by 7 | Viewed by 5115
Abstract
Asthma is a prevalent chronic non-communicable disease, affecting approximately 300 million people worldwide. It is characterized by significant airway inflammation, hyperresponsiveness, obstruction, and remodeling. Eosinophilic asthma, a subtype of asthma, involves the accumulation of eosinophils in the airways. These eosinophils release mediators and [...] Read more.
Asthma is a prevalent chronic non-communicable disease, affecting approximately 300 million people worldwide. It is characterized by significant airway inflammation, hyperresponsiveness, obstruction, and remodeling. Eosinophilic asthma, a subtype of asthma, involves the accumulation of eosinophils in the airways. These eosinophils release mediators and cytokines, contributing to severe airway inflammation and tissue damage. Emerging evidence suggests that targeting eosinophils could reduce airway remodeling and slow the progression of asthma. To achieve this, it is essential to understand the immunopathology of asthma, identify specific eosinophil-associated biomarkers, and categorize patients more accurately based on the clinical characteristics (phenotypes) and underlying pathobiological mechanisms (endotypes). This review delves into the role of eosinophils in exacerbating severe asthma, exploring various phenotypes and endotypes, as well as biomarkers. It also examines the current and emerging biological agents that target eosinophils in eosinophilic asthma. By focusing on these aspects, both researchers and clinicians can advance the development of targeted therapies to combat eosinophilic pathology in severe asthma. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms and Therapy of Asthma)
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17 pages, 1379 KiB  
Review
Regulatory ILC2—Role of IL-10 Producing ILC2 in Asthma
by Nahal Emami Fard, Maria Xiao and Roma Sehmi
Cells 2023, 12(21), 2556; https://doi.org/10.3390/cells12212556 - 31 Oct 2023
Cited by 4 | Viewed by 2676
Abstract
Over the past two decades, a growing body of evidence observations have shown group two innate lymphoid cells (ILC2) to be critical drivers of Type 2 (T2) inflammatory responses associated with allergic inflammatory conditions such as asthma. ILC2 releases copious amounts of pro-inflammatory [...] Read more.
Over the past two decades, a growing body of evidence observations have shown group two innate lymphoid cells (ILC2) to be critical drivers of Type 2 (T2) inflammatory responses associated with allergic inflammatory conditions such as asthma. ILC2 releases copious amounts of pro-inflammatory T2 cytokines—interleukin (IL)-4, IL-5, IL-9, and IL-13. This review provides a comprehensive overview of the newly discovered regulatory subtype of ILC2 described in murine and human mucosal tissue and blood. These KLRG1+ILC2 have the capacity to produce the anti-inflammatory cytokine IL-10. Papers compiled in this review were based on queries of PubMed and Google Scholar for articles published from 2000 to 2023 using keywords “IL-10” and “ILC2”. Studies with topical relevance to IL-10 production by ILC2 were included. ILC2 responds to microenvironmental cues, including retinoic acid (RA), IL-2, IL-4, IL-10, and IL-33, as well as neuropeptide mediators such as neuromedin-U (NMU), prompting a shift towards IL-10 and away from T2 cytokine production. In contrast, TGF-β attenuates IL-10 production by ILC2. Immune regulation provided by IL-10+ILC2s holds potential significance for the management of T2 inflammatory conditions. The observation of context-specific cues that alter the phenotype of ILC warrants examining characteristics of ILC subsets to determine the extent of plasticity or whether the current classification of ILCs requires refinement. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms and Therapy of Asthma)
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