Epithelial and sensory mechanisms of nasal hyperreactivity

Velasco, Enrique; Delicado‐Miralles, Miguel; Hellings, Peter; Gallar, Juana; Gerven, Laura Van; Talavera, Karel

doi:10.1111/all.15259

Cited by 17 publications

(20 citation statements)

References 103 publications

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“…Airway epithelial cells not only form a physical barrier against inhaled particles, but also recruit and activate other effector cells by producing antimicrobial peptides, chemokines, and cytokines to scavenge pathogenic insults (55). Studies have shown that the expression of TJ proteins such as claudin-1, occludin and ZO-1 is significantly reduced in patients with asthma and upper respiratory diseases such as nasal polyps and chronic rhinosinusitis (56,57). Claudin-18 expression, a TJ protein required for maintaining the integrity of the airway epithelial permeability, was also lower in asthmatics compared to healthy controls (58,59).…”

Section: Epithelial Barrier Hypothesismentioning

confidence: 99%

The External Exposome and Allergies: From the Perspective of the Epithelial Barrier Hypothesis

et al. 2022

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IntroductionIn the last decades, we have seen a rapid increase in the prevalence of allergic diseases such as asthma, allergic rhinitis, atopic dermatitis, and food allergies. The environmental changes caused by industrialization, urbanization and modernization, including dramatic increases in air pollutants such as particulate matter (PM), diesel exhaust, nitrogen dioxide (NO2), ozone (O3), alarming effects of global warming, change and loss of biodiversity, affect both human health and the entire ecosystem.ObjectiveIn this review, we aimed to discuss the effects of the external exposome on epithelial barriers and its relationship with the development of allergic diseases by considering the changes in all stakeholders of the outer exposome together, in the light of the recently proposed epithelial barrier hypothesis.MethodTo reach current, prominent, and comprehensive studies on the subject, PubMed databases were searched. We included the more resounding articles with reliable and strong results.ResultsExposure to altered environmental factors such as increased pollution, microplastics, nanoparticles, tobacco smoke, food emulsifiers, detergents, and household cleaners, and climate change, loss and change in microbial biodiversity, modifications in the consumption of dietary fatty acids, the use of emulsifiers, preservatives and the decrease in the antioxidant content of the widely consumed western diet may disrupt the epithelial barriers of the skin, respiratory and gastrointestinal tracts, making us more vulnerable to exogeneous allergens and microbes. Epithelial cell activation, microbial dysbiosis and bacterial translocation disrupt the immune balance and a chronic Th2 inflammation ensues.ConclusionDramatic increases in air pollution, worrisome effects of global warming, dysbiosis, changing dietary habits and the complex interactions of all these factors affect the epithelial barriers and local and systemic inflammation. We want to draw attention to the emerging health effects of environmental changes and to motivate the public to influence government policies for the well-being of humans and the nature of the earth and the well-being of future generations.

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Section: Epithelial Barrier Hypothesismentioning

confidence: 99%

The External Exposome and Allergies: From the Perspective of the Epithelial Barrier Hypothesis

et al. 2022

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“…More recently, neuropeptides have been reported to be involved in ILC2 activation at mucosa sites 7 . Rare neuroendocrine cells such as tuft cells and pulmonary neuroendocrine cells (PNECs) from the airway epithelial layer can secrete peptides and sense hypoxia, as well as environmental stimuli 8–10 . ILC2s selectively express the neuromedin U receptor 1 (NMUR1), and the combined expression of NMU and IL‐25, but not NMU alone, strongly promotes murine ILC2s activation induced by the house dust mite (HDM) in a cell‐intrinsic manner 11,12 .…”

Section: Pathomechanisms In Armentioning

confidence: 99%

“…7 Rare neuroendocrine cells such as tuft cells and pulmonary neuroendocrine cells (PNECs) from the airway epithelial layer can secrete peptides and sense hypoxia, as well as environmental stimuli. [8][9][10] ILC2s selectively express the neuromedin U receptor 1 (NMUR1), and the combined expression of NMU and IL-25, but not NMU alone, strongly promotes murine ILC2s activation induced by the house dust mite (HDM) in a cell-intrinsic manner. 11,12 Following OVA inhalation, murine lung PNECs release calcitonin gene-related peptide (CGRP), which can further enhance IL-5 production from ILC2s in the presence of both IL-25 and IL-33.…”

Section: New Cognition Of Ilc2s In Armentioning

confidence: 99%

Update on pathomechanisms and treatments in allergic rhinitis

Zhang

Feng

Zhang

2022

Allergy

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Allergic rhinitis (AR) is a global health problem with increasing prevalence and association with an enormous medical and socioeconomic burden. New recognition of immune cells such as type 2 innate lymphocytes (ILC2s), T helper (Th2) 2 cells, follicular helper T cells, follicular regulatory T cells, regulatory T cells, B cells, dendritic cells, and epithelial cells in AR pathogenesis has been updated in this review paper. An in‐depth understanding of the mechanisms underlying AR will aid the identification of biomarkers associated with disease and ultimately provide valuable parameters critical to guide personalized targeted therapy. As the only etiological treatment option for AR, allergen‐specific immunotherapy (AIT) has attracted increasing attention, with evidence for effectiveness of AIT recently demonstrated in several randomized controlled trials and long‐term real‐life studies. The exploration of biologics as therapeutic options has only involved anti‐IgE and anti‐type 2 inflammatory agents; however, the cost‐effectiveness of these agents remains to be elucidated precisely. In the midst of the currently on‐going COVID‐19 pandemic, a global life‐threatening disease, although some studies have indicated that AR is not a risk factor for severity and mortality of COVID‐19, this needs to be confirmed in multi‐centre, real‐life studies of AR patients from different parts of the world.

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“…A protective film composed of secretions from goblet cells, known as the mucus blanket of the nasal epithelium, forms the first barrier in nasal immunity by trapping and removing harmful substances such as dust particles, bacteria, and viruses 48–52 . The dysfunction of the nasal epithelium due to ciliary beat disorders or abnormal goblet cell secretion leads to mucous deposition and inflammation in CRS 53–56 …”

Section: Effect Of Hypoxia On Structural Cellsmentioning

confidence: 99%

“…[48][49][50][51][52] The dysfunction of the nasal epithelium due to ciliary beat disorders or abnormal goblet cell secretion leads to mucous deposition and inflammation in CRS. [53][54][55][56] Hypoxia may play a key role in the pathogenesis of CRS via nasal epithelial cells. It was previously suggested in a study by Hwang et al that the proliferation of nasal mucosal epithelial cells is inhibited under hypoxia.…”

Section: Nasal Epithelial Cellsmentioning

confidence: 99%

The role of hypoxia in the pathophysiology of chronic rhinosinusitis

Zhong

Seah

Liu

et al. 2022

Allergy

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Chronic rhinosinusitis (CRS) is characterized by inflammation of the nasal cavity and the paranasal sinuses. [1][2][3][4] It has a significant impact on living and working conditions, affecting about 5%-12% of the general population. [5][6][7] Common complaints of such patients include nasal congestion, nasal discharge, altered sense of smell, facial pain, and facial pressure. The United States conservatively estimates that spending on CRS amounts up to $30 billion each year, inevitably creating a huge economic burden on society. 7 From an etiological point of view, CRS can be classified into primary and secondary forms. 8 Primary CRS is characterized by chronic inflammation of the nasal cavity and paranasal sinuses, where an obvious secondary causative factor is absent. Secondary

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Epithelial and sensory mechanisms of nasal hyperreactivity

Cited by 17 publications

References 103 publications

The External Exposome and Allergies: From the Perspective of the Epithelial Barrier Hypothesis

The External Exposome and Allergies: From the Perspective of the Epithelial Barrier Hypothesis

Update on pathomechanisms and treatments in allergic rhinitis

The role of hypoxia in the pathophysiology of chronic rhinosinusitis

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