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A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (25 January 2022) | Viewed by 17681

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Special Issue Editor

Dr. Luisa Brussino

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Guest Editor

Department of Medical Sciences, University of Turin, 10124 Torino, Italy
Interests: asthma; allergy; COPD; immunodeficiency; connective tissue disease

Special Issue Information

Dear colleagues,

Asthma is a complex multidisciplinary disease characterized by airway inflammation and remodelling, which is frequently misdiagnosed and underrecognized, thus affecting both public health and the patient’s quality of life.

Despite many available treatments and adequate therapeutic compliance, some patients still complain of an uncontrolled, difficult to treat asthma. This has stimulated physicians and researchers to progressively improve their knowledge and identify different asthma phenotypes.

The introduction of biologic therapies as add-on treatment in severe asthma has further increased the need of novel biomarkers and asthma clustering, making the determination of asthma endotypes a key point for a tailored approach.

We are pleased to invite you to contribute to this special issue about personalized treatment for asthma. The aim of this special issue is to provide new evidence for asthma phenotyping, by finding new roles to the well-known biomarkers, as FeNO, blood eosinophils and inflammatory cytokines, and proposing new approaches in the pipeline.

I look forward to receiving your contributions.

Dr. Luisa Brussino
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. Journal of Personalized Medicine 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 2600 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.

Dr. Luisa Brussino
Guest Editor

Manuscript Submission Information

Keywords

asthma； airway inflammation； remodelling； blood eosinophils； inflammatory cytokines； biomarkers.

Published Papers (5 papers)

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Research

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10 pages, 1150 KiB

Open AccessArticle

COPD, but Not Asthma, Is Associated with Worse Outcomes in COVID-19: Real-Life Data from Four Main Centers in Northwest Italy

by Stefania Nicola, Richard Borrelli, Irene Ridolfi, Virginia Bernardi, Paolo Borrelli, Giuseppe Guida, Andrea Antonelli, Carlo Albera, Stefania Marengo, Antonio Briozzo, Claudio Norbiato, Agata Valentina Frazzetto, Marina Saad, Luca Lo Sardo, Beatrice Bacco, Silvia Gallo Cassarino, Stefano Della Mura, Diego Bagnasco, Caterina Bucca, Giovanni Rolla, Paolo Solidoro and Luisa Brussino Show full author list Hide full author list

J. Pers. Med. 2022, 12(7), 1184; https://doi.org/10.3390/jpm12071184 - 20 Jul 2022

Cited by 1 | Viewed by 1800

Abstract

Introduction: Asthma, along with inhaled steroids, was initially considered a risk factor for worse clinical outcomes in COVID-19. This was related to the higher morbidity observed in asthma patients during previous viral outbreaks. This retrospective study aimed at evaluating the prevalence of asthma among patients admitted due to SARS-CoV-2 infection as well as the impact of inhaled therapies on their outcomes. Furthermore, a comparison between patients with asthma, COPD and the general population was made. Methods: All COVID-19 inpatients were recruited between February and July 2020 from four large hospitals in Northwest Italy. Data concerning medical history, the Charlson Comorbidity Index (CCI) and the hospital stay, including length, drugs and COVID-19 complications (respiratory failure, lung involvement, and the need for respiratory support) were collected, as well as the type of discharge. Results: patients with asthma required high-flow oxygen therapy (33.3 vs. 14.3%, p = 0.001) and invasive mechanical ventilation (17.9 vs. 9.5%, p = 0.048) more frequently when compared to the general population, but no other difference was observed. Moreover, asthma patients were generally younger than patients with COPD (59.2 vs. 76.8 years, p < 0.001), they showed both a lower mortality rate (15.4 vs. 39.4%, p < 0.001) and a lower CCI (3.4 vs. 6.2, p < 0.001). Patients with asthma in regular therapy with ICS at home had significantly shorter hospital stay compared to those with no treatments (25.2 vs. 11.3 days, p = 0.024). Discussion: Our study showed that asthma is not associated with worse outcomes of COVID-19, despite the higher need for respiratory support compared with the general population, while the use of ICS allowed for a shorter hospital stay. In addition, the comparison of asthma with COPD patients confirmed the greater frailty of the latter, according to their multiple comorbidities. Full article

(This article belongs to the Special Issue Personalized Therapy of Asthma)

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19 pages, 2198 KiB

Open AccessArticle

α₄β₁ and α_Mβ₂ Integrin Expression and Pro-Proliferative Properties of Eosinophil Subtypes in Asthma

by Egle Jurkeviciute, Andrius Januskevicius, Airidas Rimkunas, Jolita Palacionyte and Kestutis Malakauskas

J. Pers. Med. 2021, 11(9), 829; https://doi.org/10.3390/jpm11090829 - 24 Aug 2021

Cited by 1 | Viewed by 2289

Abstract

Eosinophilic inflammation is one of the main pathophysiological features in asthma. Two subtypes of eosinophils exist in the lung and systemic circulation: lung-resident eosinophils (rEOS) and inflammatory eosinophils (iEOS). We evaluated the expression of α₄β₁ and α_Mβ₂ integrins of eosinophil subtypes and their influence on airway smooth muscle (ASM) cell proliferation and viability in asthma. We included 16 severe non-allergic eosinophilic asthma (SNEA) patients, 13 steroid-free, non-severe allergic asthma (AA) patients, and 12 healthy control subjects (HS). For AA patients, a bronchial allergen challenge with Dermatophagoides pteronyssinus was performed. The eosinophil subtypes were distinguished using magnetic bead-labeled antibodies against surface CD62L, and individual combined cell cultures were prepared with ASM cells. The integrins gene expression was analyzed by a quantitative real-time polymerase chain reaction. Proliferation was assessed by the Alamar blue assay, and viability by annexin V and propidium iodide staining. rEOS-like cells were characterized by the relatively higher gene expression of the β₁ integrin subunit, whereas iEOS-like cells were characterized by the α_M and β₂ integrin subunits. The inclusion of either eosinophil subtypes in co-culture significantly increased the proliferation of ASM cells, and the effect of rEOS-like cells was stronger than iEOS-like cells (p < 0.05). Furthermore, rEOS-like cells had a more pronounced effect on reducing ASM cell apoptosis compared to that of iEOS-like cells (p < 0.05). Lastly, the bronchial allergen challenge significantly enhanced only the iEOS-like cells’ effect on ASM cell proliferation and viability in AA patients (p < 0.05). These findings highlight the different expression of α₄β₁ and α_Mβ₂ integrins on distinct eosinophil subtypes in asthma. Therefore, rEOS-like cells have a stronger effect in stimulating ASM cell proliferation and viability; however, contact with specific allergens mainly enhances pro-proliferative iEOS-like cell properties. Full article

(This article belongs to the Special Issue Personalized Therapy of Asthma)

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17 pages, 1432 KiB

Open AccessArticle

Identification of ROBO2 as a Potential Locus Associated with Inhaled Corticosteroid Response in Childhood Asthma

by Natalia Hernandez-Pacheco, Mario Gorenjak, Jiang Li, Katja Repnik, Susanne J. Vijverberg, Vojko Berce, Andrea Jorgensen, Leila Karimi, Maximilian Schieck, Lesly-Anne Samedy-Bates, Roger Tavendale, Jesús Villar, Somnath Mukhopadhyay, Munir Pirmohamed, Katia M. C. Verhamme, Michael Kabesch, Daniel B. Hawcutt, Steve Turner, Colin N. Palmer, Kelan G. Tantisira, Esteban G. Burchard, Anke H. Maitland-van der Zee, Carlos Flores, Uroš Potočnik and Maria Pino-Yanes Show full author list Hide full author list

J. Pers. Med. 2021, 11(8), 733; https://doi.org/10.3390/jpm11080733 - 28 Jul 2021

Cited by 9 | Viewed by 2661

Abstract

Inhaled corticosteroids (ICS) are the most common asthma controller medication. An important contribution of genetic factors in ICS response has been evidenced. Here, we aimed to identify novel genetic markers involved in ICS response in asthma. A genome-wide association study (GWAS) of the change in lung function after 6 weeks of ICS treatment was performed in 166 asthma patients from the SLOVENIA study. Patients with an improvement in lung function ≥8% were considered as ICS responders. Suggestively associated variants (p-value ≤ 5 × 10⁻⁶) were evaluated in an independent study (n = 175). Validation of the association with asthma exacerbations despite ICS use was attempted in European (n = 2681) and admixed (n = 1347) populations. Variants previously associated with ICS response were also assessed for replication. As a result, the SNP rs1166980 from the ROBO2 gene was suggestively associated with the change in lung function (OR for G allele: 7.01, 95% CI: 3.29–14.93, p = 4.61 × 10⁻⁷), although this was not validated in CAMP. ROBO2 showed gene-level evidence of replication with asthma exacerbations despite ICS use in Europeans (minimum p-value = 1.44 × 10⁻⁵), but not in admixed individuals. The association of PDE10A-T with ICS response described by a previous study was validated. This study suggests that ROBO2 could be a potential novel locus for ICS response in Europeans. Full article

(This article belongs to the Special Issue Personalized Therapy of Asthma)

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Review

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15 pages, 763 KiB

Open AccessEditor’s ChoiceReview

Specific Therapy for T2 Asthma

by Diego Bagnasco, Elisa Testino, Stefania Nicola, Laura Melissari, Maria Russo, Rikki Frank Canevari, Luisa Brussino and Giovanni Passalacqua

J. Pers. Med. 2022, 12(4), 593; https://doi.org/10.3390/jpm12040593 - 07 Apr 2022

Cited by 8 | Viewed by 3124

Abstract

Asthma is a disease with high incidence and prevalence, and its severe form accounts for approximately 10% of asthmatics. Over the last decade, the increasing knowledge of the mechanisms underlying the disease allowed the development of biological drugs capable of sufficiently controlling symptoms and reducing the use of systemic steroids. The best-known mechanisms are those pertaining to type 2 inflammation, for which drugs were developed and studied. Those biological treatments affect crucial points of bronchial inflammation. Among the mechanisms explored, there were IgE (Omalizumab), interleukin 5 (Mepolizumab and Reslizumab), interleukin 5 receptor alpha (Benralizumab) and interleukin 4/13 receptor (Dupilumab). Under investigation and expected to be soon commercialized is the monoclonal antibody blocking the thymic stromal lymphopoietin (Tezepelumab). Seemingly under study and promising, are anti-interleukin-33 (itepekimab) and anti-suppressor of tumorigenicity-2 (astegolimab). With this study, we want to provide an overview of these drugs, paying particular attention to their mechanism of action, the main endpoints reached in clinical trials, the main results obtained in real life and some unclear points regarding their usage. Full article

(This article belongs to the Special Issue Personalized Therapy of Asthma)

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16 pages, 1426 KiB

Open AccessReview

Which Therapy for Non-Type(T)2/T2-Low Asthma

by Fabio L. M. Ricciardolo, Vitina Carriero and Francesca Bertolini

J. Pers. Med. 2022, 12(1), 10; https://doi.org/10.3390/jpm12010010 - 23 Dec 2021

Cited by 16 | Viewed by 6877

Abstract

Currently, the asthmatic population is divided into Type 2-high and non-Type 2/Type 2-low asthmatics, with 50% of patients belonging to one of the two groups. Differently from T2-high, T2-low asthma has not been clearly defined yet, and the T2-low patients are identified on the basis of the absence or non-predominant expression of T2-high biomarkers. The information about the molecular mechanisms underpinning T2-low asthma is scarce, but researchers have recognized as T2-low endotypes type 1 and type 3 immune response, and remodeling events occurring without inflammatory processes. In addition, the lack of agreed biomarkers reprents a challenge for the research of an effective therapy. The first-choice medication is represented by inhaled corticosteroids despite a low efficacy is reported for/in T2-low patients. However, macrolides and long-acting anti-muscarinic drugs have been recognized as efficacious. In recent years, clinical trials targeting biomarkers playing key roles in T3 and T1 immune pathways, alarmins, and molecules involved in neutrophil recruitment have provided conflicting results probably misleading (or biased) in patients’ selection. However, further studies are warranted to achieve a precise characterization of T2-low asthma with the aim of defining a tailored therapy for each single asthmatic patient. Full article

(This article belongs to the Special Issue Personalized Therapy of Asthma)

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