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Cells
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Mucosal Immunity in Respiratory Diseases
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Mucosal Immunity in Respiratory Diseases

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

Deadline for manuscript submissions: closed (20 November 2021) | Viewed by 19033

Special Issue Editors

Prof. Dr. Charles Pilette

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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
Prof. Dr. Antoine Froidure

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. Antoine Froidure
Guest Editors

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Published Papers (4 papers)

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Research

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16 pages, 2374 KiB  
Article
Functional Ex Vivo Testing of Alveolar Monocytes in Patients with Pneumonia-Related ARDS
by Inès Bendib, Asma Beldi-Ferchiou, Frédéric Schlemmer, Bernard Maitre, Mathieu Surenaud, Sophie Hüe, Guillaume Carteaux, Keyvan Razazi, Jean-Daniel Lelièvre, Yves Lévy, Armand Mekontso Dessap, Véronique Godot and Nicolas de Prost
Cells 2021, 10(12), 3546; https://doi.org/10.3390/cells10123546 - 15 Dec 2021
Cited by 2 | Viewed by 2830
Abstract
Biomarkers of disease severity might help with individualizing the management of patients with acute respiratory distress syndrome (ARDS). During sepsis, a sustained decreased expression of the antigen-presenting molecule human leucocyte antigen-DR (HLA-DR) on circulating monocytes is used as a surrogate marker of immune [...] Read more.
Biomarkers of disease severity might help with individualizing the management of patients with acute respiratory distress syndrome (ARDS). During sepsis, a sustained decreased expression of the antigen-presenting molecule human leucocyte antigen-DR (HLA-DR) on circulating monocytes is used as a surrogate marker of immune failure. This study aimed at assessing whether HLA-DR expression on alveolar monocytes in the setting of a severe lung infection is associated with their functional alterations. BAL fluid and blood from immunocompetent patients with pneumonia-related ARDS admitted between 2016 and 2018 were isolated in a prospective monocentric study. Alveolar and blood monocytes were immunophenotyped using flow cytometry. Functional tests were performed on alveolar and blood monocytes after in vitro lipopolysaccharide (LPS) stimulation. Phagocytosis activity and intracellular tumor necrosis factor (TNF) production were quantified using fluorochrome-conjugated-specific antibodies. Ten ARDS and seven non-ARDS control patients were included. Patients with pneumonia-related ARDS exhibited significantly lower HLA-DR expression both on circulating (p < 0.0001) and alveolar (p = 0.0002) monocytes. There was no statistically significant difference observed between patient groups (ARDS vs. non-ARDS) regarding both alveolar and blood monocytes phagocytosis activity. After LPS stimulation, alveolar (p = 0.027) and blood (p = 0.005) monocytes from pneumonia-related ARDS patients had a significantly lower intracellular TNF expression than non-ARDS patients. Monocytes from pneumonia-related ARDS patients have a deactivated status and an impaired TNF production capacity but display potent phagocytic activity. HLA-DR level expression should not be used as a surrogate marker of the phagocytic activity or the TNF production capacity of alveolar monocytes. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases)
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13 pages, 2453 KiB  
Article
Increased LGR6 Expression Sustains Long-Term Wnt Activation and Acquisition of Senescence in Epithelial Progenitors in Chronic Lung Diseases
by Emanuela E. Cortesi, Bob Meeusen, Arno Vanstapel, Stijn E. Verleden, Bart M. Vanaudenaerde, Wim A. Wuyts, Wim Janssens, Veerle Janssens, Tania Roskams and Juan-José Ventura
Cells 2021, 10(12), 3437; https://doi.org/10.3390/cells10123437 - 7 Dec 2021
Cited by 6 | Viewed by 4141
Abstract
Chronic lung diseases (CLDs) represent a set of disorders characterized by the progressive loss of proper lung function. Among severe CLDs, the incidence of chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) has grown over the last decades, mainly in the [...] Read more.
Chronic lung diseases (CLDs) represent a set of disorders characterized by the progressive loss of proper lung function. Among severe CLDs, the incidence of chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) has grown over the last decades, mainly in the elderly population. Several studies have highlighted an increased expression of senescence-related markers in the resident progenitor cells in COPD and IPF, possibly undermining epithelial integrity and contributing to the progression and the aggravation of both diseases. Recently, the chronic activation of the canonical Wnt/β-catenin pathway was shown to induce cellular senescence. Here, we investigated the localization and the expression of leucin-rich repeat-containing G-protein-coupled receptor 6 (LGR6), a protein that activates and potentiates the canonical Wnt signalling. Through immunohistochemical analyses, we identified a lesion-associated rise in LGR6 levels in abnormal lung epithelial progenitors in COPD and IPF when compared to histologically normal tissues. Moreover, in areas of aberrant regeneration, chronic damage and fibrosis, LGR6-expressing epithelial progenitors displayed a major increase in the expression of senescence-associated markers. Our study suggests the involvement of LGR6 in the chronic activation of the Wnt/β-catenin pathway, mediating the impairment and exhaustion of epithelial progenitors in COPD and IPF. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases)
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Review

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15 pages, 1029 KiB  
Review
Taste Receptors: The Gatekeepers of the Airway Epithelium
by Katleen Martens, Brecht Steelant and Dominique M. A. Bullens
Cells 2021, 10(11), 2889; https://doi.org/10.3390/cells10112889 - 26 Oct 2021
Cited by 9 | Viewed by 4028
Abstract
Taste receptors are well known for their role in the sensation of taste. Surprisingly, the expression and involvement of taste receptors in chemosensory processes outside the tongue have been recently identified in many organs including the airways. Currently, a clear understanding of the [...] Read more.
Taste receptors are well known for their role in the sensation of taste. Surprisingly, the expression and involvement of taste receptors in chemosensory processes outside the tongue have been recently identified in many organs including the airways. Currently, a clear understanding of the airway-specific function of these receptors and the endogenous activating/inhibitory ligands is lagging. The focus of this review is on recent physiological and clinical data describing the taste receptors in the airways and their activation by secreted bacterial compounds. Taste receptors in the airways are potentially involved in three different immune pathways (i.e., the production of nitric oxide and antimicrobial peptides secretion, modulation of ciliary beat frequency, and bronchial smooth muscle cell relaxation). Moreover, genetic polymorphisms in these receptors may alter the patients’ susceptibility to certain types of respiratory infections as well as to differential outcomes in patients with chronic inflammatory airway diseases such as chronic rhinosinusitis and asthma. A better understanding of the function of taste receptors in the airways may lead to the development of a novel class of therapeutic molecules that can stimulate airway mucosal immune responses and could treat patients with chronic airway diseases. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases)
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15 pages, 10024 KiB  
Review
Alveolar Macrophages: Adaptation to Their Anatomic Niche during and after Inflammation
by Florian Pierre Martin, Cédric Jacqueline, Jeremie Poschmann and Antoine Roquilly
Cells 2021, 10(10), 2720; https://doi.org/10.3390/cells10102720 - 12 Oct 2021
Cited by 25 | Viewed by 7036
Abstract
At the early stages of life development, alveoli are colonized by embryonic macrophages, which become resident alveolar macrophages (ResAM) and self-sustain by local division. Genetic and epigenetic signatures and, to some extent, the functions of ResAM are dictated by the lung microenvironment, which [...] Read more.
At the early stages of life development, alveoli are colonized by embryonic macrophages, which become resident alveolar macrophages (ResAM) and self-sustain by local division. Genetic and epigenetic signatures and, to some extent, the functions of ResAM are dictated by the lung microenvironment, which uses cytokines, ligand-receptor interactions, and stroma cells to orchestrate lung homeostasis. In resting conditions, the lung microenvironment induces in ResAM a tolerogenic programming that prevents unnecessary and potentially harmful inflammation responses to the foreign bodies, which continuously challenge the airways. Throughout life, any episode of acute inflammation, pneumonia being likely the most frequent cause, depletes the pool of ResAM, leaving space for the recruitment of inflammatory monocytes that locally develop in monocyte-derived alveolar macrophages (InfAM). During lung infection, the local microenvironment induces a temporary inflammatory signature to the recruited InfAM to handle the tissue injury and eliminate the pathogens. After a few days, the recruited InfAM, which locally self-sustain and develop as new ResAM, gain profibrotic functions required for tissue healing. After the complete resolution of the infectious episode, the functional programming of both embryonic and monocyte-derived ResAM remains altered for months and possibly for the entire life. Adult lungs thus contain a wide diversity of ResAM since every infection brings new waves of InfAM which fill the room left open by the inflammatory process. The memory of these innate cells called trained immunity constitutes an immunologic scar left by inflammation, notably pneumonia. This memory of ResAM has advantages and drawbacks. In some cases, lung-trained immunity offers better defense capacities against autoimmune disorders and the long-term risk of infection. At the opposite, it can perpetuate a harmful process and lead to a pathological state, as is the case among critically ill patients who have immune paralysis and are highly susceptible to hospital-acquired pneumonia and acute respiratory distress syndrome. The progress in understanding the kinetics of response of alveolar macrophages (AM) to lung inflammation is paving the way to new treatments of pneumonia and lung inflammatory process. Full article
(This article belongs to the Special Issue Mucosal Immunity in Respiratory Diseases)
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