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8.3
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Journals
Biomolecules
Special Issues
The Role of Epithelial Cells in Airway Diseases
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The Role of Epithelial Cells in Airway Diseases

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 3163

Special Issue Editors

Dr. Giusy Daniela Albano

E-Mail Website
Guest Editor
CNR - Istituto di Farmacologia Traslazionale, Palermo, Italy
Interests: airway diseases; epithelial cells; cell models; biomarkers; inflammation; oxidative stress
Dr. Mirella Profita

E-Mail Website
Guest Editor
CNR—Istituto di Farmacologia Traslazionale, Palermo, Italy
Interests: airway diseases; epithelial cells; cell models; biomarkers; inflammation; oxidative stress

Special Issue Information

Dear Colleagues,

The airway epithelium is a barrier between the environment and lung. It is a dynamic tissue that undergoes slow but constant renewal. It is the first line of defense against environmental stimuli such as cigarette smoke, allergens, microbes, and pollutants circulating in the air. The airway epithelium plays many important functions including barrier protection, fluid balance, and clearance of particulate, and contributes to both innate and adaptive immune function in the lower respiratory tract, mucus and surfactant production, and repair following injury. It contributes to both innate and adaptive immune functions in the lower respiratory tract.

Barrier dysfunction might facilitate the entrance of foreign substances, initiating and facilitating the onset of lung disease, and increasing susceptibility to respiratory infections, thereby increasing the risk of exacerbations and triggering further inflammation. All of this can induce the onset of many respiratory diseases such as COPD, asthma, fibrosis, cancer, and other disorders.

The aim of this Special issue is to examine pathophysiological processes and their related mechanisms in epithelial cells and/or to identify new and innovative therapeutic target for airway diseases.

Dr. Giusy Daniela Albano
Dr. Mirella Profita
Guest Editors

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

  • airway diseases
  • epithelial cells
  • cell models
  • biomarkers
  • epithelial dysfunction

Published Papers (2 papers)

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Review

12 pages, 9661 KiB  
Review
Multifactorial Causes and Consequences of TLSP Production, Function, and Release in the Asthmatic Airway
by Danica L. Brister, Hafsa Omer, Christiane E. Whetstone, Maral Ranjbar and Gail M. Gauvreau
Biomolecules 2024, 14(4), 401; https://doi.org/10.3390/biom14040401 - 26 Mar 2024
Viewed by 760
Abstract
Disruption of the airway epithelium triggers a defensive immune response that begins with the production and release of alarmin cytokines. These epithelial-derived alarmin cytokines, including thymic stromal lymphopoietin (TSLP), are produced in response to aeroallergens, viruses, and toxic inhalants. An alarmin response disproportionate [...] Read more.
Disruption of the airway epithelium triggers a defensive immune response that begins with the production and release of alarmin cytokines. These epithelial-derived alarmin cytokines, including thymic stromal lymphopoietin (TSLP), are produced in response to aeroallergens, viruses, and toxic inhalants. An alarmin response disproportionate to the inhaled trigger can exacerbate airway diseases such as asthma. Allergens inhaled into previously sensitized airways are known to drive a T2 inflammatory response through the polarization of T cells by dendritic cells mediated by TSLP. Harmful compounds found within air pollution, microbes, and viruses are also triggers causing airway epithelial cell release of TSLP in asthmatic airways. The release of TSLP leads to the development of inflammation which, when unchecked, can result in asthma exacerbations. Genetic and inheritable factors can contribute to the variable expression of TSLP and the risk and severity of asthma. This paper will review the various triggers and consequences of TSLP release in asthmatic airways. Full article
(This article belongs to the Special Issue The Role of Epithelial Cells in Airway Diseases)
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21 pages, 2913 KiB  
Review
Autophagy/Mitophagy in Airway Diseases: Impact of Oxidative Stress on Epithelial Cells
by Giusy Daniela Albano, Angela Marina Montalbano, Rosalia Gagliardo and Mirella Profita
Biomolecules 2023, 13(8), 1217; https://doi.org/10.3390/biom13081217 - 4 Aug 2023
Cited by 3 | Viewed by 1949
Abstract
Autophagy is the key process by which the cell degrades parts of itself within the lysosomes. It maintains cell survival and homeostasis by removing molecules (particularly proteins), subcellular organelles, damaged cytoplasmic macromolecules, and by recycling the degradation products. The selective removal or degradation [...] Read more.
Autophagy is the key process by which the cell degrades parts of itself within the lysosomes. It maintains cell survival and homeostasis by removing molecules (particularly proteins), subcellular organelles, damaged cytoplasmic macromolecules, and by recycling the degradation products. The selective removal or degradation of mitochondria is a particular type of autophagy called mitophagy. Various forms of cellular stress (oxidative stress (OS), hypoxia, pathogen infections) affect autophagy by inducing free radicals and reactive oxygen species (ROS) formation to promote the antioxidant response. Dysfunctional mechanisms of autophagy have been found in different respiratory diseases such as chronic obstructive lung disease (COPD) and asthma, involving epithelial cells. Several existing clinically approved drugs may modulate autophagy to varying extents. However, these drugs are nonspecific and not currently utilized to manipulate autophagy in airway diseases. In this review, we provide an overview of different autophagic pathways with particular attention on the dysfunctional mechanisms of autophagy in the epithelial cells during asthma and COPD. Our aim is to further deepen and disclose the research in this direction to stimulate the develop of new and selective drugs to regulate autophagy for asthma and COPD treatment. Full article
(This article belongs to the Special Issue The Role of Epithelial Cells in Airway Diseases)
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