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Article ; Online: Epithelial dysfunction in chronic respiratory diseases, a shared endotype?

Steelant, Brecht

2019 Volume 26, Issue 1, Page(s) 20–26

Abstract: Purpose of review: Epithelial barrier defects are being appreciated in various inflammatory disorders; however, causal underlying mechanisms are lacking. In this review, we describe the disruption of the airway epithelium with regard to upper and lower ... ...

Abstract	Purpose of review: Epithelial barrier defects are being appreciated in various inflammatory disorders; however, causal underlying mechanisms are lacking. In this review, we describe the disruption of the airway epithelium with regard to upper and lower airway diseases, the role of epigenetic alterations underlying this process, and potential novel ways of interfering with dysfunctional epithelial barriers as a novel therapeutic approach. Recent findings: A defective epithelial barrier, impaired innate defence mechanisms or hampered epithelial cell renewal are found in upper and lower airway diseases. Barrier dysfunction might facilitate the entrance of foreign substances, initiating and facilitating the onset of disease. Latest data provided novel insights for possible involvement of epigenetic alterations induced by inflammation or other unknown mechanisms as a potential mechanism responsible for epithelial defects. Additionally, these mechanisms might precede disease development, and represent a novel therapeutic approach for restoring epithelial defects. Summary: A better understanding of the role of epigenetics in driving and maintaining epithelial defects in various inflammatory diseases, using state-of-the-art biology tools will be crucial in designing novel therapies to protect or reconstitute a defective airway epithelial barrier.
MeSH term(s)	Blood-Air Barrier/physiology ; Blood-Air Barrier/physiopathology ; Epigenesis, Genetic ; Humans ; Inflammation ; Respiratory Mucosa/physiology ; Respiratory Mucosa/physiopathology ; Respiratory Tract Diseases/genetics ; Respiratory Tract Diseases/immunology
Language	English
Publishing date	2019-11-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1285505-4
ISSN	1531-6971 ; 1070-5287 ; 1078-1641
ISSN (online)	1531-6971
ISSN	1070-5287 ; 1078-1641
DOI	10.1097/MCP.0000000000000638
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Article: Validation and shortcomings of the most common mouse model of chronic rhinosinusitis with nasal polyps

Sánchez-Montalvo, A / Lecocq, M / Bouillet, E / Steelant, B / Gohy, S / Froidure, A / Bullens, D / Pilette, C / Hox, V

Rhinology

2024

Abstract: Background: Chronic rhinosinusitis (CRS) is a highly prevalent airway disease worldwide. Whereas eosinophilic CRS with nasal polyps (eCRSwNP) represents its most severe phenotype, pathogenic mechanisms remain poorly understood despite a wide spectrum of ...

Abstract	Background: Chronic rhinosinusitis (CRS) is a highly prevalent airway disease worldwide. Whereas eosinophilic CRS with nasal polyps (eCRSwNP) represents its most severe phenotype, pathogenic mechanisms remain poorly understood despite a wide spectrum of in vitro and in vivo experimental models. A mouse model of experimental ovalbumin (OVA)-induced airway allergy with coadministration of Staphylococcus aureus enterotoxin B (SEB) has been widely used to study eosinophilic eCRSwNP. This study revisits the features of this model and its suitability for studying eCRS. Methodology: We implemented the most used eCRSwNP mouse model based on OVA+SEB intranasal challenges. Readouts including inflammatory features by (immuno)histology of the sinonasal epithelium (NP formation, eosinophils, epithelial and basement membrane thickness, fibrosis, goblet cells, Charcot-Leyden crystals (CLC)-like, tight junctions) and IgE production by enzyme-linked immunosorbent assay (ELISA), were compared to features of the corresponding human disease. Results: The OVA+SEB model induced eosinophilic inflammation of upper and lower airways, with epithelial and basement membrane thickening, goblet cell hyperplasia and subepithelial fibrosis in the sinuses, along increased IgE production. Except local IgE in nasal lavage (NL), which was only increased in OVA+SEB group, all other features did not differ between OVA and OVA+SEB groups. Macro- or microscopic NP were not detected. Conclusions: With the notable exception of local IgE production, the addition of SEB did not induce additional inflammatory or structural change in the sinuses from mice exposed to and challenged with OVA. This model might represent a model for severe upper airway allergy rather than a specific model of human eCRSwNP.
Language	English
Publishing date	2024-03-18
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80336-4
ISSN	0300-0729
ISSN	0300-0729
DOI	10.4193/Rhin23.331
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Article ; Online: Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?

Van Broeck, Dorien / Steelant, Brecht / Scadding, Glenis / Hellings, Peter W

Frontiers in allergy

2023 Volume 4, Page(s) 1080951

Abstract: Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a clinical syndrome characterized by nasal polyposis, asthma, and intolerance to aspirin/NSAID. It affects approximately 15% cases of severe asthma, 10% of nasal ... ...

Abstract	Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a clinical syndrome characterized by nasal polyposis, asthma, and intolerance to aspirin/NSAID. It affects approximately 15% cases of severe asthma, 10% of nasal polyps and 9% of rhinosinusitis. N-ERD results in associated asthma exacerbations, oral corticosteroids bursts, corticosteroid-dependent disease, and multiple endoscopic sinus surgeries. Unknown influences cause polyp epithelium to release alarmins, such as IL-33 and TSLP. These cytokines activate lymphoid cells, both Th2 and ILC2, to release cytokines such as IL5, IL4 and IL13, resulting in complex type 2 inflammation involving mast cells, eosinophils and platelets. Arachidonic acid released from such cells is metabolized into mediators. N-ERD is characterized by an imbalance in eicosanoid levels, especially CysLTs, PDG and PGE2. Patients with N-ERD present nasal symptoms (congestion, hyposmia/anosmia, nasal discharge) and lower airways symptoms (cough, sneezing, shortness of breath, chest tightness), anosmia, severe hyposmia as well as severe asthma which impacts the quality of life in this disease and leads to safety concerns in patients daily lives. Despite the variety of treatment strategies, the likelihood of recurrence of symptoms is high in patients with N-ERD. The most important strategies for treating N-ERD are listed as following: drug therapies, aspirin desensitization, monoclonal antibodies and other therapies associated. N-ERD treatment remains a major challenge in the current situation. Selecting the appropriate patient for aspirin desensitization, monoclonal antibodies or both is essential. This review provides an overview on aspirin desensitization and biologics in N-ERD and might help in decision making from both the perspective of the physician and patient. Patient characteristics, safety, efficacy, health care costs, but also patient preferences are all factors to take into account when it comes to a choice between biologics or aspirin desensitization.
Language	English
Publishing date	2023-04-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ISSN	2673-6101
ISSN (online)	2673-6101
DOI	10.3389/falgy.2023.1080951
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Article: Nasal hyperreactivity in allergic rhinitis and chronic rhinosinusitis with polyps: a role for neuronal pathways.

Backaert, W / Steelant, B / Wils, T / Qian, Z / Dilissen, E / Jonckheere, A-C / Boonen, B / Jorissen, M / Schrijvers, R / Bullens, M A / Talavera, K / Hellings, P W / Van Gerven, L

Rhinology

2024

Abstract: Background: Nasal hyperreactivity (NHR) is prevalent in all chronic upper airway inflammatory phenotypes, including allergic rhinitis (AR) and chronic rhinosinusitis with nasal polyps (CRSwNP). Although NHR in patients with non-allergic rhinitis is ... ...

Abstract	Background: Nasal hyperreactivity (NHR) is prevalent in all chronic upper airway inflammatory phenotypes, including allergic rhinitis (AR) and chronic rhinosinusitis with nasal polyps (CRSwNP). Although NHR in patients with non-allergic rhinitis is mediated by neuronal pathways, AR and CRSwNP are mainly characterized by type 2 inflammation. Methods: Eighteen healthy controls and 45 patients with symptomatic AR/CRSwNP underwent a cold, dry air (CDA) provocation test for objective diagnosis of NHR. Before and after, questionnaires were filled out and nasal secretions and biopsies were collected. Markers for neurogenic inflammation (substance P, calcitonin gene-related peptide, neurokinin A), epithelial activation (IL-33), and histamine were measured in secretions by ELISA; and expression of neuronal markers PGP9.5, TRPV1, and TRPM8 was studied in biopsies by RT-q-PCR. Effects of histamine on TRPV1/A1 were studied with Ca2+-imaging using murine trigeminal neurons. Results: CDA-provocation reduced peak nasal inspiratory flow (PNIF) of patients with subjective NHR but not of non-NHR controls/ patients (p.
Language	English
Publishing date	2024-02-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80336-4
ISSN	0300-0729
ISSN	0300-0729
DOI	10.4193/Rhin23.287
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Article ; Online: Epithelial barriers in allergy and asthma.

Hellings, Peter W / Steelant, Brecht

The Journal of allergy and clinical immunology

2020 Volume 145, Issue 6, Page(s) 1499–1509

Abstract: The respiratory epithelium provides a physical, functional, and immunologic barrier to protect the host from the potential harming effects of inhaled environmental particles and to guarantee maintenance of a healthy state of the host. When compromised, ... ...

Abstract	The respiratory epithelium provides a physical, functional, and immunologic barrier to protect the host from the potential harming effects of inhaled environmental particles and to guarantee maintenance of a healthy state of the host. When compromised, activation of immune/inflammatory responses against exogenous allergens, microbial substances, and pollutants might occur, rendering individuals prone to develop chronic inflammation as seen in allergic rhinitis, chronic rhinosinusitis, and asthma. The airway epithelium in asthma and upper airway diseases is dysfunctional due to disturbed tight junction formation. By putting the epithelial barrier to the forefront of the pathophysiology of airway inflammation, different approaches to diagnose and target epithelial barrier defects are currently being developed. Using single-cell transcriptomics, novel epithelial cell types are being unraveled that might play a role in chronicity of respiratory diseases. We here review and discuss the current understandings of epithelial barrier defects in type 2-driven chronic inflammation of the upper and lower airways, the estimated contribution of these novel identified epithelial cells to disease, and the current clinical challenges in relation to diagnosis and treatment of allergic rhinitis, chronic rhinosinusitis, and asthma.
MeSH term(s)	Allergens/immunology ; Animals ; Asthma/immunology ; Epithelial Cells/immunology ; Humans ; Hypersensitivity/immunology ; Inflammation/immunology ; Respiratory Mucosa/immunology ; Respiratory System/immunology
Chemical Substances	Allergens
Keywords	covid19
Language	English
Publishing date	2020-06-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2020.04.010
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Article ; Online: Nasal hyperreactivity in rhinitis: A diagnostic and therapeutic challenge.

Van Gerven, L / Steelant, B / Hellings, P W

Allergy

2018 Volume 73, Issue 9, Page(s) 1784–1791

Abstract: Although nasal hyperreactivity (NHR) is a common feature in patients suffering from allergic and nonallergic rhinitis, it is widely neglected during history taking, underdiagnosed in the majority of patients with rhinitis and rhinosinusitis, not ... ...

Abstract	Although nasal hyperreactivity (NHR) is a common feature in patients suffering from allergic and nonallergic rhinitis, it is widely neglected during history taking, underdiagnosed in the majority of patients with rhinitis and rhinosinusitis, not considered as an outcome parameter in clinical trials on novel treatments for rhinitis and rhinosinusitis, and no target for routine treatment. In contrast to the simple nature of diagnosing NHR by a history of nasal symptoms induced by nonspecific exogenous and/or endogenous triggers, quantification is hardly performed in routine clinic given the lack of a simple tool for its diagnosis. So far, limited efforts have been invested into gaining better insight in the underlying pathophysiology of NHR, helping us to explain why some patients with inflammation develop NHR and others not. Of note, environmental and microbial factors have been reported to influence NHR, contributing to the complex nature of understanding the development of NHR. As a consequence of the neglect of NHR as a key clinical feature of rhinitis and chronic rhinosinusitis (CRS), patients with NHR might be suboptimally controlled and/or dissatisfied with current treatment. We here aim to provide a comprehensive overview of current knowledge on the pathophysiology, and the available tools to diagnose and treat NHR.
MeSH term(s)	Bronchial Hyperreactivity/diagnosis ; Bronchial Hyperreactivity/epidemiology ; Bronchial Hyperreactivity/etiology ; Bronchial Hyperreactivity/therapy ; Bronchial Provocation Tests/methods ; Humans ; Nasal Mucosa/immunology ; Rhinitis/diagnosis ; Rhinitis/epidemiology ; Rhinitis/etiology ; Rhinitis/therapy
Language	English
Publishing date	2018-04-22
Publishing country	Denmark
Document type	Journal Article ; Review
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.13453
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Article: Determination of the chronic upper airway inflammatory phenotype using a symptom-score-based algorithm.

Backaert, W / Steelant, B / Guler, I / Talavera, K / Jorissen, M / Schrijvers, R / Hellings, P W / Van Gerven, L

Rhinology

2022 Volume 61, Issue 1, Page(s) 90–92

MeSH term(s)	Humans ; Phenotype ; Algorithms
Language	English
Publishing date	2022-10-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80336-4
ISSN	0300-0729
ISSN	0300-0729
DOI	10.4193/Rhin22.141
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Article ; Online: Taste Receptors: The Gatekeepers of the Airway Epithelium.

Martens, Katleen / Steelant, Brecht / Bullens, Dominique M A

Cells

2021 Volume 10, Issue 11

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. ... ...

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 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.
MeSH term(s)	Animals ; Epithelium/metabolism ; Humans ; Models, Biological ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Respiratory System/metabolism ; Respiratory System/pathology ; Taste
Chemical Substances	Receptors, G-Protein-Coupled
Language	English
Publishing date	2021-10-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10112889
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Article ; Online: Airway Basal Cells, Protectors of Epithelial Walls in Health and Respiratory Diseases.

Ruysseveldt, Emma / Martens, Katleen / Steelant, Brecht

Frontiers in allergy

2021 Volume 2, Page(s) 787128

Abstract: The airway epithelium provides a critical barrier to the outside environment. When its integrity is impaired, epithelial cells and residing immune cells collaborate to exclude pathogens and to heal tissue damage. Healing is achieved through tissue- ... ...

Abstract	The airway epithelium provides a critical barrier to the outside environment. When its integrity is impaired, epithelial cells and residing immune cells collaborate to exclude pathogens and to heal tissue damage. Healing is achieved through tissue-specific stem cells: the airway basal cells. Positioned near the basal membrane, airway basal cells sense and respond to changes in tissue health by initiating a pro-inflammatory response and tissue repair via complex crosstalks with nearby fibroblasts and specialized immune cells. In addition, basal cells have the capacity to learn from previous encounters with the environment. Inflammation can indeed imprint a certain memory on basal cells by epigenetic changes so that sensitized tissues may respond differently to future assaults and the epithelium becomes better equipped to respond faster and more robustly to barrier defects. This memory can, however, be lost in diseased states. In this review, we discuss airway basal cells in respiratory diseases, the communication network between airway basal cells and tissue-resident and/or recruited immune cells, and how basal cell adaptation to environmental triggers occurs.
Language	English
Publishing date	2021-11-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ISSN	2673-6101
ISSN (online)	2673-6101
DOI	10.3389/falgy.2021.787128
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Article ; Online: The nasal basal cell population shifts towards a diseased phenotype with impaired barrier formation capacity in allergic rhinitis.

Ruysseveldt, Emma / Steelant, Brecht / Wils, Tine / Cremer, Jonathan / Bullens, Dominique M A / Hellings, Peter W / Martens, Katleen

The Journal of allergy and clinical immunology

2024

Abstract: Background: The integrity of the airway epithelium is guarded by the airway basal cells that serve as progenitor cells and restore wounds in case of injury. Basal cells are a heterogenous population and specific changes in their behavior are associated ... ...

Abstract	Background: The integrity of the airway epithelium is guarded by the airway basal cells that serve as progenitor cells and restore wounds in case of injury. Basal cells are a heterogenous population and specific changes in their behavior are associated with chronic barrier disruption; mechanisms that have not been studied in detail in allergic rhinitis (AR). Objective: We here aim to study basal cell (sub)types in AR and healthy controls. Methods: scRNAseq of the nasal epithelium was performed on non-allergic and house dust mite allergic AR patients to reveal basal cell diversity and to identify allergy-related alterations. Flow cytometry, immunofluorescence staining and in vitro experiments using primary basal cells were performed to confirm phenotypic findings at protein level and functionally. Results: scRNAseq, flow cytometry and immunofluorescence staining revealed that basal cells are abundantly and heterogeneously present in the nasal epithelium, suggesting specialized subtypes. The total basal cell fraction within the epithelium in AR is increased compared to controls. scRNAseq demonstrated that potentially beneficial basal cells are missing in AR epithelium, while an activated population of allergy-associated basal cells is more dominantly present. Furthermore, our in vitro proliferation, wound healing assay and ALI cultures show that AR-associated basal cells have altered progenitor capacity compared with non-allergic basal cells. Conclusions: The nasal basal cell population is abundant, diverse and shifts towards a diseased state in AR. The absence of potentially protective subtypes and the rise of a pro-inflammatory population suggest that basal cells are important players in maintaining epithelial barrier defects in AR.
Language	English
Publishing date	2024-05-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2024.04.021
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