Mucosal Immunity in Respiratory Diseases Ⅱ

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 23084

Special Issue Editors


E-Mail Website
Guest Editor
Department of Respiratory Medicine, Cliniques Universitaires St-Luc and institute of Experimental and Clinical Research, Université Catholique de Louvain (UCL), 10 Avenue Hippocrate, B-1200 Brussels, Belgium
Interests: mucosal immunology; respiratory medicine; allergy and pulmonary diseases; IgA; lung epithelium biology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Respiratory Medicine, Cliniques Universitaires St-Luc and institute of Experimental and Clinical Research, Université Catholique de Louvain (UCL), 10 Avenue Hippocrate, B-1200 Brussels, Belgium
Interests: dendritic cells; allergic asthma; pulmonary fibrosis; interstitial lung disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The upper airways and lungs are directly exposed to external matters. This environmental pressure represents a challenge for the respiratory epithelial barrier and the immune system in order to prevent unnecessary responses and to adapt their responses to noxious or harmless exposures. Homeostasis at the mucosal barriers involves a complex interplay between structural and immune cells, an emerging concept in which the “memory” of previous responses are developed not only in immune cells, but also in epithelial stem cells. Asthma and chronic obstructive pulmonary disease (COPD) are major pulmonary diseases, prototypically linked with abnormal lung responses to inhaled allergens or toxics (e.g., cigarette smoke), respectively. They share longstanding histories of repeated exposure-response phases over years that may cause alterations in airway development, epithelial–mesenchymal unit biology, and chronic immune activation. Altered mucosal immunity (notably its major mediator, namely IgA) integrates the pathophysiology of chronic respiratory diseases and could reflect an abnormal interplay in the airway/lung microbiome. This phenomenon is also observed during cystic fibrosis, a genetic disease of the epithelium, and pulmonary fibrosis, a progressive disease of senescent lungs. In addition, early dysregulation of mucosal immunity may imprint the airways during childhood, thus promoting future asthma development. An integrated view of mucosal (dys)immunity in the lungs should offer valuable targets for preventive or therapeutic interventions in order to tackle pathogenic mechanisms before irreversible changes feed the roots of chronic disease.

Prof. Dr. Charles Pilette
Prof. Dr. Antoine Froidure
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.

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (5 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

12 pages, 2617 KiB  
Article
Salvia miltiorrhiza Bunge as a Potential Natural Compound against COVID-19
by Simon J. L. Petitjean, Marylène Lecocq, Camille Lelong, Robin Denis, Sylvie Defrère, Pierre-Antoine Mariage, David Alsteens and Charles Pilette
Cells 2022, 11(8), 1311; https://doi.org/10.3390/cells11081311 - 12 Apr 2022
Cited by 20 | Viewed by 4404
Abstract
Salvia miltiorrhiza Bunge, commonly called danshen, is widely used in traditional Chinese medicine for its cardiovascular and neuroprotective effects, which include antioxidative, anti-inflammatory, and antifibrotic properties. The purpose of this study was to evaluate the preclinical potential of S. miltiorrhiza extracts for the [...] Read more.
Salvia miltiorrhiza Bunge, commonly called danshen, is widely used in traditional Chinese medicine for its cardiovascular and neuroprotective effects, which include antioxidative, anti-inflammatory, and antifibrotic properties. The purpose of this study was to evaluate the preclinical potential of S. miltiorrhiza extracts for the treatment of COVID-19. First, the impact of the extract on the binding between SARS-CoV-2 and the cellular ACE2 receptors was assessed using atomic force microscopy (AFM), showing a significant reduction in binding by the extract at concentrations in the µg/mL range. Second, the interference of this extract with the inflammatory response of blood mononuclear cells (PBMCs) was determined, demonstrating potent inhibitory properties in the same concentration range on pro-inflammatory cytokine release and interference with the activation of NFκB signaling. Together, these in vitro data demonstrate the potential of S. miltiorrhiza against COVID-19, consisting first of the blockade of the binding of SARS-CoV-2 to the ACE2 receptor and the mitigation of the inflammatory response from leukocytes by interfering with NFκB signaling. This dataset prompts the launch of a clinical trial to address in vivo the clinical benefits of this promising agent. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases Ⅱ)
Show Figures

Figure 1

Review

Jump to: Research

31 pages, 1617 KiB  
Review
The Dual Role of the Airway Epithelium in Asthma: Active Barrier and Regulator of Inflammation
by Andreas Frey, Lars P. Lunding and Michael Wegmann
Cells 2023, 12(18), 2208; https://doi.org/10.3390/cells12182208 - 5 Sep 2023
Cited by 3 | Viewed by 2870
Abstract
Chronic airway inflammation is the cornerstone on which bronchial asthma arises, and in turn, chronic inflammation arises from a complex interplay between environmental factors such as allergens and pathogens and immune cells as well as structural cells constituting the airway mucosa. Airway epithelial [...] Read more.
Chronic airway inflammation is the cornerstone on which bronchial asthma arises, and in turn, chronic inflammation arises from a complex interplay between environmental factors such as allergens and pathogens and immune cells as well as structural cells constituting the airway mucosa. Airway epithelial cells (AECs) are at the center of these processes. On the one hand, they represent the borderline separating the body from its environment in order to keep inner homeostasis. The airway epithelium forms a multi-tiered, self-cleaning barrier that involves an unstirred, discontinuous mucous layer, the dense and rigid mesh of the glycocalyx, and the cellular layer itself, consisting of multiple, densely interconnected cell types. On the other hand, the airway epithelium represents an immunologically highly active tissue once its barrier has been penetrated: AECs play a pivotal role in releasing protective immunoglobulin A. They express a broad spectrum of pattern recognition receptors, enabling them to react to environmental stressors that overcome the mucosal barrier. By releasing alarmins—proinflammatory and regulatory cytokines—AECs play an active role in the formation, strategic orientation, and control of the subsequent defense reaction. Consequently, the airway epithelium is of vital importance to chronic inflammatory diseases, such as asthma. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases Ⅱ)
Show Figures

Figure 1

19 pages, 864 KiB  
Review
Role of Respiratory Epithelial Cells in Allergic Diseases
by Constanze A. Jakwerth, Jose Ordovas-Montanes, Simon Blank, Carsten B. Schmidt-Weber and Ulrich M. Zissler
Cells 2022, 11(9), 1387; https://doi.org/10.3390/cells11091387 - 20 Apr 2022
Cited by 19 | Viewed by 4799
Abstract
The airway epithelium provides the first line of defense to the surrounding environment. However, dysfunctions of this physical barrier are frequently observed in allergic diseases, which are tightly connected with pro- or anti-inflammatory processes. When the epithelial cells are confronted with allergens or [...] Read more.
The airway epithelium provides the first line of defense to the surrounding environment. However, dysfunctions of this physical barrier are frequently observed in allergic diseases, which are tightly connected with pro- or anti-inflammatory processes. When the epithelial cells are confronted with allergens or pathogens, specific response mechanisms are set in motion, which in homeostasis, lead to the elimination of the invaders and leave permanent traces on the respiratory epithelium. However, allergens can also cause damage in the sensitized organism, which can be ascribed to the excessive immune reactions. The tight interaction of epithelial cells of the upper and lower airways with local and systemic immune cells can leave an imprint that may mirror the pathophysiology. The interaction with effector T cells, along with the macrophages, play an important role in this response, as reflected in the gene expression profiles (transcriptomes) of the epithelial cells, as well as in the secretory pattern (secretomes). Further, the storage of information from past exposures as memories within discrete cell types may allow a tissue to inform and fundamentally alter its future responses. Recently, several lines of evidence have highlighted the contributions from myeloid cells, lymphoid cells, stromal cells, mast cells, and epithelial cells to the emerging concepts of inflammatory memory and trained immunity. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases Ⅱ)
Show Figures

Figure 1

18 pages, 1697 KiB  
Review
Secretory Immunoglobulin A Immunity in Chronic Obstructive Respiratory Diseases
by Charlotte de Fays, François M. Carlier, Sophie Gohy and Charles Pilette
Cells 2022, 11(8), 1324; https://doi.org/10.3390/cells11081324 - 13 Apr 2022
Cited by 18 | Viewed by 5217
Abstract
Chronic obstructive pulmonary disease (COPD), asthma and cystic fibrosis (CF) are distinct respiratory diseases that share features such as the obstruction of small airways and disease flare-ups that are called exacerbations and are often caused by infections. Along the airway epithelium, immunoglobulin (Ig) [...] Read more.
Chronic obstructive pulmonary disease (COPD), asthma and cystic fibrosis (CF) are distinct respiratory diseases that share features such as the obstruction of small airways and disease flare-ups that are called exacerbations and are often caused by infections. Along the airway epithelium, immunoglobulin (Ig) A contributes to first line mucosal protection against inhaled particles and pathogens. Dimeric IgA produced by mucosal plasma cells is transported towards the apical pole of airway epithelial cells by the polymeric Ig receptor (pIgR), where it is released as secretory IgA. Secretory IgA mediates immune exclusion and promotes the clearance of pathogens from the airway surface by inhibiting their adherence to the epithelium. In this review, we summarize the current knowledge regarding alterations of the IgA/pIgR system observed in those major obstructive airway diseases and discuss their implication for disease pathogenesis. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases Ⅱ)
Show Figures

Figure 1

23 pages, 1409 KiB  
Review
Extracellular Lipids in the Lung and Their Role in Pulmonary Fibrosis
by Olivier Burgy, Sabrina Loriod, Guillaume Beltramo and Philippe Bonniaud
Cells 2022, 11(7), 1209; https://doi.org/10.3390/cells11071209 - 3 Apr 2022
Cited by 19 | Viewed by 5178
Abstract
Lipids are major actors and regulators of physiological processes within the lung. Initial research has described their critical role in tissue homeostasis and in orchestrating cellular communication to allow respiration. Over the past decades, a growing body of research has also emphasized how [...] Read more.
Lipids are major actors and regulators of physiological processes within the lung. Initial research has described their critical role in tissue homeostasis and in orchestrating cellular communication to allow respiration. Over the past decades, a growing body of research has also emphasized how lipids and their metabolism may be altered, contributing to the development and progression of chronic lung diseases such as pulmonary fibrosis. In this review, we first describe the current working model of the mechanisms of lung fibrogenesis before introducing lipids and their cellular metabolism. We then summarize the evidence of altered lipid homeostasis during pulmonary fibrosis, focusing on their extracellular forms. Finally, we highlight how lipid targeting may open avenues to develop therapeutic options for patients with lung fibrosis. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases Ⅱ)
Show Figures

Figure 1

Back to TopTop