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Cells
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Molecular and Cellular Mechanism of Airway Diseases
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Molecular and Cellular Mechanism of Airway Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: closed (15 June 2022) | Viewed by 24560

Special Issue Editors

Prof. Dr. Gabriela Krasteva-Christ

E-Mail Website1 Website2
Guest Editor
Department of Anatomy, Institute of Anatomy and Cell Biology, University of Saarland, 66424 Homburg, Germany
Interests: airway diseases
Prof. Dr. Christoph Beisswenger

E-Mail Website
Guest Editor
Department of Internal Medicine V-Pulmonology, Allergology, Respiratory and Environmental Medicine, Saarland University, 66424 Homburg, Germany
Interests: airway diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic airway diseases have a high incidence and prevalence worldwide. Molecules as diverse as miRNAs, cytokines, or peptides, along with a plethora of inflammatory, epithelial, mesenchymal, and smooth muscle cells, contribute to the development and progression of airway diseases. Even though diseases such as asthma, COPD, and cystic fibrosis share common characteristics (e.g., limitation of the airflow, chronic inflammation, mucus production), the pathophysiology behind and the clinical outcomes differ. Still today, the molecular and cellular mechanisms driving disease progression are insufficiently understood, and treatment options need to be improved. The multifactorial nature of airway diseases and the lack of standardized translational models pose an additional enormous challenge for the development of successful therapeutic approaches.

Recent advances in technology, such as single-cell sequencing and organoid cultures, and the generation of a plethora of mutant and transgenic mouse lines allow studying the function of molecular mechanisms and interactions of a broad spectrum of molecules and cell types in the pathogenesis of airway diseases. Here, we would like to provide a platform for sharing new research that sheds light on the complexity of airway diseases, for conceptual and technological innovation in these field and new therapeutic targets.

This Special Issue encourages the submission of original research articles, reviews or methodological articles dealing with various aspects of airway disease. Contributions may address but are not limited to airway injury and repair mechanisms, genetic polymorphisms, altered immune responses, and infection, as well as novel molecular or cellular targets for therapeutic interventions. Studies with clear translational potential are especially welcome.

We look forward to your contributions.

Prof. Dr. Gabriela Krasteva-Christ
Prof. Dr. Christoph Beisswenger
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. Cells is an international peer-reviewed open access semimonthly 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

  • airways
  • signaling pathway
  • disease models
  • transgenic mouse lines/reporter tools
  • cell signaling

Published Papers (7 papers)

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Research

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19 pages, 3774 KiB  
Article
Taste Receptor Activation in Tracheal Brush Cells by Denatonium Modulates ENaC Channels via Ca2+, cAMP and ACh
by Monika I. Hollenhorst, Praveen Kumar, Maxim Zimmer, Alaa Salah, Stephan Maxeiner, Mohamed Ibrahem Elhawy, Saskia B. Evers, Veit Flockerzi, Thomas Gudermann, Vladimir Chubanov, Ulrich Boehm and Gabriela Krasteva-Christ
Cells 2022, 11(15), 2411; https://doi.org/10.3390/cells11152411 - 04 Aug 2022
Cited by 4 | Viewed by 2455
Abstract
Mucociliary clearance is a primary defence mechanism of the airways consisting of two components, ciliary beating and transepithelial ion transport (ISC). Specialised chemosensory cholinergic epithelial cells, named brush cells (BC), are involved in regulating various physiological and immunological processes. However, it [...] Read more.
Mucociliary clearance is a primary defence mechanism of the airways consisting of two components, ciliary beating and transepithelial ion transport (ISC). Specialised chemosensory cholinergic epithelial cells, named brush cells (BC), are involved in regulating various physiological and immunological processes. However, it remains unclear if BC influence ISC. In murine tracheae, denatonium, a taste receptor agonist, reduced basal ISC in a concentration-dependent manner (EC50 397 µM). The inhibition of bitter taste signalling components with gallein (Gβγ subunits), U73122 (phospholipase C), 2-APB (IP3-receptors) or with TPPO (Trpm5, transient receptor potential-melastatin 5 channel) reduced the denatonium effect. Supportively, the ISC was also diminished in Trpm5−/− mice. Mecamylamine (nicotinic acetylcholine receptor, nAChR, inhibitor) and amiloride (epithelial sodium channel, ENaC, antagonist) decreased the denatonium effect. Additionally, the inhibition of Gα subunits (pertussis toxin) reduced the denatonium effect, while an inhibition of phosphodiesterase (IBMX) increased and of adenylate cyclase (forskolin) reversed the denatonium effect. The cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor CFTRinh172 and the KCNQ1 potassium channel antagonist chromanol 293B both reduced the denatonium effect. Thus, denatonium reduces ISC via the canonical bitter taste signalling cascade leading to the Trpm5-dependent nAChR-mediated inhibition of ENaC as well as Gα signalling leading to a reduction in cAMP-dependent ISC. Therefore, BC activation contributes to the regulation of fluid homeostasis. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanism of Airway Diseases)
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19 pages, 7273 KiB  
Article
Pseudomonas aeruginosa Alters Critical Lung Epithelial Cell Functions through Activation of ADAM17
by Ahmad Aljohmani, Noah Niklas Andres and Daniela Yildiz
Cells 2022, 11(15), 2303; https://doi.org/10.3390/cells11152303 - 26 Jul 2022
Cited by 3 | Viewed by 2279
Abstract
Severe epithelial dysfunction is one major hallmark throughout the pathophysiological progress of bacterial pneumonia. Junctional and cellular adhesion molecules (e.g., JAMA-A, ICAM-1), cytokines (e.g., TNFα), and growth factors (e.g., TGFα), controlling proper lung barrier function and leukocyte recruitment, are proteolytically cleaved and released [...] Read more.
Severe epithelial dysfunction is one major hallmark throughout the pathophysiological progress of bacterial pneumonia. Junctional and cellular adhesion molecules (e.g., JAMA-A, ICAM-1), cytokines (e.g., TNFα), and growth factors (e.g., TGFα), controlling proper lung barrier function and leukocyte recruitment, are proteolytically cleaved and released into the extracellular space through a disintegrin and metalloproteinase (ADAM) 17. In cell-based assays, we could show that the protein expression, maturation, and activation of ADAM17 is upregulated upon infection of lung epithelial cells with Pseudomonas aeruginosa and Exotoxin A (ExoA), without any impact of infection by Streptococcus pneumoniae. The characterization of released extracellular vesicles/exosomes and the comparison to heat-inactivated bacteria revealed that this increase occurred in a cell-associated and toxin-dependent manner. Pharmacological targeting and gene silencing of ADAM17 showed that its activation during infection with Pseudomonas aeruginosa was critical for the cleavage of junctional adhesion molecule A (JAM-A) and epithelial cell survival, both modulating barrier integrity, epithelial regeneration, leukocyte adhesion and transepithelial migration. Thus, site-specific targeting of ADAM17 or blockage of the activating toxins may constitute a novel anti-infective therapeutic option in Pseudomonas aeruginosa lung infection preventing severe epithelial and organ dysfunctions and stimulating future translational studies. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanism of Airway Diseases)
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17 pages, 2498 KiB  
Article
Neutrophil-Derived Extracellular Vesicles Activate Platelets after Pneumolysin Exposure
by Eleftheria Letsiou, Luiz Gustavo Teixeira Alves, Matthias Felten, Timothy J. Mitchell, Holger C. Müller-Redetzky, Steven M. Dudek and Martin Witzenrath
Cells 2021, 10(12), 3581; https://doi.org/10.3390/cells10123581 - 18 Dec 2021
Cited by 13 | Viewed by 3374
Abstract
Pneumolysin (PLY) is a pore-forming toxin of Streptococcus pneumoniae that contributes substantially to the inflammatory processes underlying pneumococcal pneumonia and lung injury. Host responses against S. pneumoniae are regulated in part by neutrophils and platelets, both individually and in cooperative interaction. Previous studies [...] Read more.
Pneumolysin (PLY) is a pore-forming toxin of Streptococcus pneumoniae that contributes substantially to the inflammatory processes underlying pneumococcal pneumonia and lung injury. Host responses against S. pneumoniae are regulated in part by neutrophils and platelets, both individually and in cooperative interaction. Previous studies have shown that PLY can target both neutrophils and platelets, however, the mechanisms by which PLY directly affects these cells and alters their interactions are not completely understood. In this study, we characterize the effects of PLY on neutrophils and platelets and explore the mechanisms by which PLY may induce neutrophil–platelet interactions. In vitro studies demonstrated that PLY causes the formation of neutrophil extracellular traps (NETs) and the release of extracellular vesicles (EVs) from both human and murine neutrophils. In vivo, neutrophil EV (nEV) levels were increased in mice infected with S. pneumoniae. In platelets, treatment with PLY induced the cell surface expression of P-selectin (CD62P) and binding to annexin V and caused a significant release of platelet EVs (pl-EVs). Moreover, PLY-induced nEVs but not NETs promoted platelet activation. The pretreatment of nEVs with proteinase K inhibited platelet activation, indicating that the surface proteins of nEVs play a role in this process. Our findings demonstrate that PLY activates neutrophils and platelets to release EVs and support an important role for neutrophil EVs in modulating platelet functions in pneumococcal infections. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanism of Airway Diseases)
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Review

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20 pages, 793 KiB  
Review
Transient Receptor Potential (TRP) Channels in Airway Toxicity and Disease: An Update
by Isabel Müller, Philipp Alt, Suhasini Rajan, Lena Schaller, Fabienne Geiger and Alexander Dietrich
Cells 2022, 11(18), 2907; https://doi.org/10.3390/cells11182907 - 17 Sep 2022
Cited by 12 | Viewed by 3463
Abstract
Our respiratory system is exposed to toxicants and pathogens from both sides: the airways and the vasculature. While tracheal, bronchial and alveolar epithelial cells form a natural barrier in the airways, endothelial cells protect the lung from perfused toxic compounds, particulate matter and [...] Read more.
Our respiratory system is exposed to toxicants and pathogens from both sides: the airways and the vasculature. While tracheal, bronchial and alveolar epithelial cells form a natural barrier in the airways, endothelial cells protect the lung from perfused toxic compounds, particulate matter and invading microorganism in the vascular system. Damages induce inflammation by our immune response and wound healing by (myo)fibroblast proliferation. Members of the transient receptor potential (TRP) superfamily of ion channel are expressed in many cells of the respiratory tract and serve multiple functions in physiology and pathophysiology. TRP expression patterns in non-neuronal cells with a focus on TRPA1, TRPC6, TRPM2, TRPM5, TRPM7, TRPV2, TRPV4 and TRPV6 channels are presented, and their roles in barrier function, immune regulation and phagocytosis are summarized. Moreover, TRP channels as future pharmacological targets in chronic obstructive pulmonary disease (COPD), asthma, cystic and pulmonary fibrosis as well as lung edema are discussed. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanism of Airway Diseases)
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16 pages, 4223 KiB  
Review
IL-17 Cytokines and Chronic Lung Diseases
by Felix Ritzmann, Lars Peter Lunding, Robert Bals, Michael Wegmann and Christoph Beisswenger
Cells 2022, 11(14), 2132; https://doi.org/10.3390/cells11142132 - 06 Jul 2022
Cited by 28 | Viewed by 4289
Abstract
IL-17 cytokines are expressed by numerous cells (e.g., gamma delta (γδ) T, innate lymphoid (ILC), Th17, epithelial cells). They contribute to the elimination of bacteria through the induction of cytokines and chemokines which mediate the recruitment of inflammatory cells to the site of [...] Read more.
IL-17 cytokines are expressed by numerous cells (e.g., gamma delta (γδ) T, innate lymphoid (ILC), Th17, epithelial cells). They contribute to the elimination of bacteria through the induction of cytokines and chemokines which mediate the recruitment of inflammatory cells to the site of infection. However, IL-17-driven inflammation also likely promotes the progression of chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), lung cancer, cystic fibrosis, and asthma. In this review, we highlight the role of IL-17 cytokines in chronic lung diseases. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanism of Airway Diseases)
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12 pages, 1643 KiB  
Review
COVID-19 and Liquid Homeostasis in the Lung—A Perspective through the Epithelial Sodium Channel (ENaC) Lens
by Emily F. Brown, Tamapuretu Mitaera and Martin Fronius
Cells 2022, 11(11), 1801; https://doi.org/10.3390/cells11111801 - 31 May 2022
Cited by 4 | Viewed by 4431
Abstract
Infections with a new corona virus in 2019 lead to the definition of a new disease known as Corona Virus Disease 2019 (COVID-19). The sever cases of COVID-19 and the main cause of death due to virus infection are attributed to respiratory distress. [...] Read more.
Infections with a new corona virus in 2019 lead to the definition of a new disease known as Corona Virus Disease 2019 (COVID-19). The sever cases of COVID-19 and the main cause of death due to virus infection are attributed to respiratory distress. This is associated with the formation of pulmonary oedema that impairs blood oxygenation and hypoxemia as main symptoms of respiratory distress. An important player for the maintenance of a defined liquid environment in lungs needed for normal lung function is the epithelial sodium channel (ENaC). The present article reviews the implications of SARS-CoV-2 infections from the perspective of impaired function of ENaC. The rationale for this perspective is derived from the recognition that viral spike protein and ENaC share a common proteolytic cleavage site. This cleavage site is utilized by the protease furin, that is essential for ENaC activity. Furin cleavage of spike ‘activates’ the virus protein to enable binding to host cell membrane receptors and initiate cell infection. Based on the importance of proteolytic cleavage for ENaC function and activation of spike, it seems feasible to assume that virus infections are associated with impaired ENaC activity. This is further supported by symptoms of COVID-19 that are reminiscent of impaired ENaC function in the respiratory tract. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanism of Airway Diseases)
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17 pages, 1940 KiB  
Review
The Role of Extracellular Vesicles in Idiopathic Pulmonary Fibrosis Progression: An Approach on Their Therapeutics Potential
by Alma Aurora Ramírez-Hernández, Juan Manuel Velázquez-Enríquez, Jovito Cesar Santos-Álvarez, Armando López-Martínez, Edilburga Reyes-Jiménez, Gabriela Carrasco-Torres, Karina González-García, Verónica Rocío Vásquez-Garzón and Rafael Baltierrez-Hoyos
Cells 2022, 11(4), 630; https://doi.org/10.3390/cells11040630 - 11 Feb 2022
Cited by 6 | Viewed by 3402
Abstract
Idiopathic pulmonary fibrosis (IPF) is a fibrosing interstitial lung disease of unknown etiology. Different types of cells are involved in fibrogenesis, which is persistently physical and molecular stimulation, either directly or by interacting with bioactive molecules and extracellular vesicles (EVs). Current evidence suggests [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a fibrosing interstitial lung disease of unknown etiology. Different types of cells are involved in fibrogenesis, which is persistently physical and molecular stimulation, either directly or by interacting with bioactive molecules and extracellular vesicles (EVs). Current evidence suggests that EVs play an essential role in IPF development. EVs are released by a variety of cells, including fibroblasts, epithelial cells, and alveolar macrophages. In addition, EVs can transport bioactive molecules, such as lipids, proteins, and nucleic acids, which play a pivotal role in cellular communication. Several proposed mechanisms show that an acceptor cell can capture, absorb, or interact with EVs through direct fusion with the plasma membrane, ligand–receptor interaction, and endocytotic process, modifying the target cell. During fibrogenesis, the release of EVs is deregulated, increases the EVs amount, and the cargo content is modified. This alteration is closely associated with the maintenance of the fibrotic microenvironment. This review summarizes the current data on the participation of EVs secreted by the cells playing a critical role in IPF pathogenesis. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanism of Airway Diseases)
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