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Biomarkers of Severe Asthma: From Pathogenetic Mechanisms to Clinical Application

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A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biomarkers".

Deadline for manuscript submissions: closed (15 January 2024) | Viewed by 5457

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Special Issue Editor

Prof. Dr. Alessandro Vatrella

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Guest Editor

Department of Medicine, Surgery and Dentistry, University of Salerno, Salerno, Italy
Interests: severe asthma; biomarkers; biologics; airway inflammation; OCS dependent asthma

Special Issue Information

Dear Colleagues,

Asthma is a chronic respiratory disease characterized by variable symptoms of wheezing, shortness of breath, chest tightness, cough, and variable expiratory airflow limitation. It is usually associated with airway hyper-responsiveness and chronic inflammation of the airways. Although most patients achieve good symptom control using drugs such as inhaled corticosteroids and bronchodilators, there is a percentage of patients who, despite optimized treatments, do not reach a satisfactory clinical control, requiring the use of additional resources both in terms of direct and indirect costs.

In recent years, the deepening of knowledge on the etiopathogenetic mechanisms underlying the different phenotypes and endotypes of asthma has led to the possibility of developing extremely refined pharmacological treatments that are capable of intercepting specific molecular inflammatory pathways, with the potential aim of modifying the natural history of the disease. Most of these drugs are currently available for the treatment of the type 2 asthma endotype; however, drugs that target the so-called alarmins have very recently been developed, and act upstream of the type 2 inflammatory cascade. The ability of these drugs to substantially change the daily lives of patients who use them has allowed clinicians to identify the best outcomes capable of quantifying the degree of response to these treatments. Among the response parameters, the concentration of specific biomarkers has been included to predict asthma outcomes and therapeutic response to targeted therapies.

In recent years, significant research has been realized in the identification of valid biomarkers for asthma. This Special Issue focuses on the existent and emerging biomarkers with clinical higher applicability in the management of asthma.

Prof. Dr. Alessandro Vatrella
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 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. Biomolecules 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 2700 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

severe asthma
OCS-dependent asthma
asthma control
airway inflammation
biologic drugs
asthma biomarkers
asthma exacerbations

Published Papers (4 papers)

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Research

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15 pages, 1765 KiB

Open AccessArticle

MiRNA and Exosomal miRNA as New Biomarkers Useful to Phenotyping Severe Asthma

by Piera Soccio, Giorgia Moriondo, Donato Lacedonia, Pasquale Tondo, Dalila Pescatore, Carla Maria Irene Quarato, Mauro Carone, Maria Pia Foschino Barbaro and Giulia Scioscia

Biomolecules 2023, 13(10), 1542; https://doi.org/10.3390/biom13101542 - 18 Oct 2023

Cited by 2 | Viewed by 1236

Abstract

Severe asthma (SA) is a chronic inflammatory disease of the airways. Due to the extreme heterogeneity of symptoms, new biomarkers are currently needed. MiRNAs are non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. In biological fluids, miRNAs are contained within exosomes, vesicles capable of giving miRNAs considerable stability and resistance to degradation by RNAses. The main function attributed to the exosomes is intercellular communication. The goal of our study was to analyze intracellular and exosomal miRNAs in order to demonstrate their potential use as non-invasive biomarkers of asthma by showing, in particular, their role in SA. We detected miRNAs by qRT-PCR in both serum and serum-derived-exosomes of asthmatic patients and healthy controls. The levels of almost all analyzed intracellular miRNAs (miR-21, miR-223, and let-7a) were greater in asthmatic patients vs. healthy control, except for miR-223. In detail, miR-21 was greater in SA, while let-7a increased in mild-to-moderate asthma. On the other hand, in exosomes, all analyzed miRNAs were higher in SA. This study identified a series of miRNAs involved in SA, highlighting their potential role in asthma development and progression. These results need validation on a larger cohort. Full article

(This article belongs to the Special Issue Biomarkers of Severe Asthma: From Pathogenetic Mechanisms to Clinical Application)

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11 pages, 2115 KiB

Open AccessArticle

Type 2 Low Biomarker Stability and Exacerbations in Severe Uncontrolled Asthma

by Arja Viinanen, Juhani Aakko, Mariann I. Lassenius, Gunilla Telg, Kaisa Nieminen, Saara Kaijala, Lauri Lehtimäki and Hannu Kankaanranta

Biomolecules 2023, 13(7), 1118; https://doi.org/10.3390/biom13071118 - 13 Jul 2023

Cited by 3 | Viewed by 1987

Abstract

We investigated the stability of T2 low status, based on low levels of T2 biomarkers, and exacerbation rates in T2 low and non-T2 low asthma from clinical retrospective data of severe uncontrolled asthma patients. Knowledge of the T2 low biomarker profile is sparse and biomarker stability is uncharted. Secondary care patients with severe uncontrolled asthma and at least two blood eosinophil counts (BEC) and fractional exhaled nitric oxide (FeNO) measured for determination of type 2 inflammation status were evaluated from a follow-up period of 4 years. Patients were stratified into four groups: T2 low₁₅₀ (n = 31; BEC < 150 cells/µL and FeNO < 25 ppb), non-T2 low₁₅₀ (n = 138; BEC > 150 cells/µL and/or FeNO > 25 ppb), T2 low₃₀₀ (n = 66; BEC < 300 cells/µL and FeNO < 25 ppb), and non-T2 low₃₀₀ (n = 103; BEC > 300 cells/µL and/or FeNO > 25 ppb). Exacerbation rates requiring hospital care, stability of biomarker status, and cumulative OCS and ICS doses were assessed during follow-up. Among patients with severe uncontrolled asthma, 18% (n = 31) were identified as T2 low₁₅₀, and 39% (n = 66) as T2 low₃₀₀. In these groups, the low biomarker profile was stable in 55% (n = 11) and 72% (n = 33) of patients with follow-up measures. Exacerbation rates were different between the T2 low and non-T2 low groups: 19.7 [95% CI: 4.3–45.6] in T2 low₁₅₀ vs. 8.4 [4.7–13.0] in non-T2 low₁₅₀ per 100 patient-years. BEC and FeNO are useful biomarkers in identifying T2 low severe uncontrolled asthma, showing a stable follow-up biomarker profile in up to 72% of patients. Repeated monitoring of these biomarkers is essential in identifying and treating patients with T2 low asthma. Full article

(This article belongs to the Special Issue Biomarkers of Severe Asthma: From Pathogenetic Mechanisms to Clinical Application)

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Review

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18 pages, 806 KiB

Open AccessReview

The Exploitation of the Glycosylation Pattern in Asthma: How We Alter Ancestral Pathways to Develop New Treatments

by Angelika Muchowicz, Agnieszka Bartoszewicz and Zbigniew Zaslona

Biomolecules 2024, 14(5), 513; https://doi.org/10.3390/biom14050513 - 24 Apr 2024

Viewed by 588

Abstract

Asthma has reached epidemic levels, yet progress in developing specific therapies is slow. One of the main reasons for this is the fact that asthma is an umbrella term for various distinct subsets. Due to its high heterogeneity, it is difficult to establish biomarkers for each subset of asthma and to propose endotype-specific treatments. This review focuses on protein glycosylation as a process activated in asthma and ways to utilize it to develop novel biomarkers and treatments. We discuss known and relevant glycoproteins whose functions control disease development. The key role of glycoproteins in processes integral to asthma, such as inflammation, tissue remodeling, and repair, justifies our interest and research in the field of glycobiology. Altering the glycosylation states of proteins contributing to asthma can change the pathological processes that we previously failed to inhibit. Special emphasis is placed on chitotriosidase 1 (CHIT1), an enzyme capable of modifying LacNAc- and LacdiNAc-containing glycans. The expression and activity of CHIT1 are induced in human diseased lungs, and its pathological role has been demonstrated by both genetic and pharmacological approaches. We propose that studying the glycosylation pattern and enzymes involved in glycosylation in asthma can help in patient stratification and in developing personalized treatment. Full article

(This article belongs to the Special Issue Biomarkers of Severe Asthma: From Pathogenetic Mechanisms to Clinical Application)

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19 pages, 1584 KiB

Open AccessReview

TNF Superfamily and ILC2 Activation in Asthma

by Takahiro Matsuyama, Brittany Marie Salter, Nahal Emami Fard, Kentaro Machida and Roma Sehmi

Biomolecules 2024, 14(3), 294; https://doi.org/10.3390/biom14030294 - 29 Feb 2024

Viewed by 1144

Abstract

Eosinophilic asthma is the most prevalent and well-defined phenotype of asthma. Despite a majority of patients responding to corticosteroid therapy and T2 biologics, there remains a subset that have recurrent asthma exacerbations, highlighting a need for additional therapies to fully ameliorate airway eosinophilia. Group 2 innate lymphoid cells (ILC2) are considered key players in the pathogenesis of eosinophilic asthma through the production of copious amounts of type 2 cytokines, namely IL-5 and IL-13. ILC2 numbers are increased in the airways of asthmatics and with the greatest numbers of activated ILC2 detected in sputa from severe prednisone-dependent asthma with uncontrolled eosinophilia. Although epithelial-derived cytokines are important mediators of ILC2 activation, emerging evidence suggests that additional pathways stimulate ILC2 function. The tumor necrosis factor super family (TNFSF) and its receptors (TNFRSF) promote ILC2 activity. In this review, we discuss evidence supporting a relationship between ILC2 and TNFSF/TNFRSF axis in eosinophilic asthma and the role of this relationship in severe asthma with airway autoimmune responses. Full article

(This article belongs to the Special Issue Biomarkers of Severe Asthma: From Pathogenetic Mechanisms to Clinical Application)

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