Journal of Asthma and Allergy

Dove Medical Press is pleased to invite you to submit your research to the upcoming Article Collection “Atopic Dermatitis and Other Atopic Comorbidities” in the Journal of Asthma and Allergy.

Atopic dermatitis (AD) is a chronic inflammatory cutaneous disorder. Currently, AD has been found to be associated with substantial patient burden and numerous atopic comorbidities, including asthma, allergic rhinitis, food allergy, and eosinophilic esophagitis, as well as nonatopic comorbidities, including allergic contact dermatitis, anxiety, depression, suicidality, infections, and cardiovascular disease. All these comorbidities led to the recognition of AD as a systemic disease. Of note, the relationship between AD and comorbidities is likely bidirectional and multifactorial, as well as some comorbidities may be secondary to the effects of the burden of chronic AD.

This Article Collection aims to explore the association between atopic dermatitis and other atopic comorbidities, shedding light on the shared pathophysiological mechanisms and the implications for clinical management.

This Article Collection aims to bring together original research articles, review articles, and commentaries exploring the pathogenesis of atopic diseases, also considering primary immune defects presenting as AD, the role of environmental factors, the impact of environmental allergies and infections, novel diagnostic approaches (including biomarkers), and emerging therapeutic approaches (including biologic treatments and JAK inhibitors). Articles regarding all the atopic diseases (asthma, food allergy, allergic rhinitis, eosinophilic esophagitis, and atopic dermatitis) are welcome.

Potential topics include the following aspects:
- Epidemiology and burden of atopic comorbidities
- Pathophysiological mechanisms
- The role of environmental allergies in atopic diseases
- Biomarkers in atopic diseases
- Asthma and allergic rhinitis in atopic dermatitis
- Atopic dermatitis and food allergies
- Atopic dermatitis and mental health
- Novel therapeutic approaches
- The use of biologics in atopic diseases
- Clinical management and guidelines

All manuscripts submitted to this Article Collection will undergo desk assessment and peer-review as part of our standard editorial process. Guest Advisors for this collection will not be involved in peer-reviewing manuscripts unless they are an existing member of the Editorial Board. Please review the journal Aims and Scope and author submission instructions prior to submitting a manuscript.

The deadline for submissions is 19 April 2024.

Please submit your manuscript on our website, quoting the promo code DFHHN to indicate that your submission is for consideration in this Article Collection.

Guest Advisors
Maddalena Napolitano, Professor, MD, Section of Dermatology, Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy
[email protected]

Luca Potestio, MD, Section of Dermatology, Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy
[email protected]

Cataldo Patruno, Professor, MD, Department of Health Sciences, University Magna Graecia of Catanzaro, Catanzaro
[email protected]

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Dove Medical Press is pleased to invite you to submit your research to the upcoming Article Collection “New Promising Treatments for Type 2 and Non-Type 2 Asthma” in the Journal of Asthma and Allergy.

Although the hallmark of asthma pathobiology is airway inflammation, asthma is highly heterogeneous and is thus characterized by a variety of distinct symptoms supported by elaborate endotype networks of cellular and molecular systems. 

Type 2 (T2) asthma is the most common phenotype/endotype; it may affect both atopic and non-atopic individuals and is primarily maintained by bronchial eosinophilic inflammation. T2-low inflammation, particularly defined by neutrophilic or mixed (eosinophilic-neutrophilic) cellular infiltration of the airways, is present in a significant portion of asthmatic patients. Neutrophil illness is reliant on the cooperative synergy of innate and adaptive immunological responses, much like eosinophilic asthma. 

Paucigranulocytic (non-T2) asthma is a different phenotype/endotype that is likely characterized by a predominance of involvement of airway structure cells, such as epithelial cells and particularly smooth muscle cells. 

These physiological and molecular pathways that underlie airway inflammation in asthma define the targets of the current asthma treatments. Inhaled corticosteroids, which have the ability to block the biological activities of a number of immune-inflammatory cells as well as the generation of a large number of cytokines and chemokines, are the cornerstone of the therapy of asthma. However, severe asthma may also be steroid-insensitive to varying degrees. Therefore, monoclonal antibodies that target IgE, pro-inflammatory cytokines, or their receptors are the basis of add-on biological therapy for T2-high severe asthma. Nowadays, omalizumab (anti-IgE), mepolizumab (anti-IL5), reslizumab (anti-IL5), benralizumab (anti-IL5R), dupilumab (anti-IL4/13R) and tezepelumab (anti-TSLP) are available for the treatment of T2-high asthma. Unfortunately, fewer therapeutic opportunities are authorized to treat T2-low severe asthma. 

The goal of this Article Collection is to summarize recent developments pertaining to the inflammatory pathways underlying the phenotypes and endotypes of asthma. Clarifying the cellular and molecular targets of pharmacological therapies for this pervasive illness depends on ongoing work in this area. 

All manuscripts submitted to this Article Collection will undergo a full peer-review; the Guest Advisors for this Collection will not be handling the manuscripts (unless they are an Editorial Board member). Please review the journal scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website, quoting the promo code PAGBV to indicate that your submission is for consideration in this Article Collection.

The deadline for submitting manuscripts is 19 April 2024. For questions about this Article Collection, including inquiries regarding discounts off of the article publishing charges, please contact Commissioning Editor Dr. MK Huffman at [email protected]. 

Guest Advisors

Corrado Pelaia, University "Magna Graecia" of Catanzaro

[email protected]

My research interests primarily deal with the pathobiology of asthma and the biological therapies of severe asthma. In particular, I am especially interested in the cellular and molecular mechanisms underlying the development of type 2 inflammation in asthma, as well as in the current knowledge and future perspectives regarding add-on biological treatment of uncontrolled asthma. Therefore, my research interests span both clinical activity and basic science. In particular, my work experiences include the diagnostic and therapeutic management of patients with respiratory diseases, and the laboratory techniques applied to the proteomic and peptidomic analysis of induced sputum, blood, and other biological samples. 

Angelantonio Maglio, University of Salerno

[email protected]

My clinical activity is mainly focused on the treatment of patients with both common and rare pulmonary diseases. In the last few years, I worked in a specialized referral centre for the diagnosis and treatment of severe asthma, idiopathic pulmonary fibrosis, and other rare respiratory diseases.

My research work focused particularly on the fields of obstructive lung diseases, with contributions to the understanding and management of asthma and COPD. My main research topics include the role of inflammation in asthma, anti-inflammatory treatment in asthma and COPD, brand-new biological therapies in severe asthma, and the search for affordable biomarkers of disease activity and severity. My clinical and research time is supplemented and integrated by didactical activity within PhD courses in Translational and Clinical Medicine.

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Dove Medical Press is pleased to invite you to submit your research to the upcoming Article Collection “From Guts to Lungs: Understanding Microbiome Dynamics in Respiratory Health” in the Journal of Asthma and Allergy.

Globally, chronic respiratory diseases pose a major public health problem. In 2017, chronic respiratory diseases attributed to approximately 3.91 million (7%) of worldwide deaths. Common chronic diseases of the upper and lower respiratory tract include cystic fibrosis (CF), chronic rhinosinusitis (CRS), asthma, and chronic obstructive pulmonary disorder (COPD). These diseases affect individuals differentially across the lifespan. 

CF is caused by genetic mutations to the CFTR gene. Recent advances in CFTR modulating therapeutics have improved patient’s quality of life and lifespan. More than half of the CF population is age 18 or older. Childhood asthma contributes to significant morbidity worldwide, and incidence is increasing, particularly in industrialized populations. CRS is a major cause of morbidity in the adult population, affecting between 5%-10% of adults. COPD, the third leading cause of death in the United States, is typically diagnosed later in adulthood, though early onset COPD may be more common than previously recognized. 

Though not an exhaustive list, these chronic diseases present a significant burden to patients and the healthcare system. Risk factors for onset or severity tend to include environment and sociodemographic factors that have an impact on gut and respiratory microbiome composition and function. The host microbiome, or the trillions of microbes that colonize distinct body sites, has a critical role in health status. Studies of the gut microbiome in respiratory disease demonstrate that gut microbiota are critical modulators of inflammatory pathways in the airways, and this can be influenced by environmental factors, such as diet. It is critical to understand 1) how microbiome-host interactions contribute to chronic inflammation in the upper and lower airways, and 2) how age-associated changes in the microbiome, shaped by the host and environment, contribute to development or severity of respiratory diseases. In this Article Collection, we are interested in manuscripts that broadly explore these topics, with emphasis on the following: 

• Chronic respiratory diseases and the airway microbiome (e.g., sinus microbiome composition, airway microbiome interactions)

• Chronic respiratory diseases and the gut microbiome (e.g., gut microbiome-lung axis in asthma; dietary habits on gut microbiome or GI morbidities in respiratory disease)

• Insights into host-microbiome interactions at the airway mucosa and via the gut microbiome-airway axis (e.g., modulation of type 2 immunity in the lungs by respiratory or gut microbiota; microbial metabolites and immune signaling; epigenetic regulation of host-microbiome interaction)

• Early-life development of the microbiome and asthma risk (e.g., early life microbial exposures and asthma susceptibility; household microbial exposures in early infancy)

• Health disparities focused on microbiome-targeted interventions or insights (e.g., intersectionality in health disparities and the combined impact of social determinants and microbiome in airway disease; microbiome-mediate effects of access to healthcare and airway disease outcomes)

• Novel technologies (e.g., single cell sequencing, integrated omics, microfluidics)

All manuscripts submitted to this Article Collection will undergo a full peer-review; the Guest Advisors for this Collection will not be handling the manuscripts (unless they are an Editorial Board member). Please review the journal scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website, quoting the promo code VTXKB to indicate that your submission is for consideration in this Article Collection.

The deadline for submitting manuscripts is 17 May 2024. For questions about this Article Collection, including inquiries regarding discounts off of the article publishing charges, please contact Commissioning Editor Dr. MK Huffman at [email protected].

Guest Advisor

Emily Cope, Associate Professor, Northern Arizona University

[email protected]

Dr. Emily Cope is an Associate Professor of Biological Sciences at Northern Arizona University (NAU) and Assistant Director of the Pathogen and Microbiome Institute at NAU. Her research program focuses on the role of the microbiome, specifically microbiome-host interactions, in chronic and progressive diseases.

 

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