Global Airway Disease Beyond Allergy

Hellings, Peter W.; Prokopakis, Emmanuel P.

doi:10.1007/s11882-010-0107-1

Cited by 46 publications

(31 citation statements)

References 31 publications

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“…The "united airways concept" (Figure 2) implies that besides the anatomical continuity of the upper and lower airways, inflammation in one part of the airway influences the homeostasis of the other (27) . The mechanisms underlying this interaction have been studied primarily in allergic disease, showing systemic immune activation, induction of inflammation at a distance, and a negative impact of nasal inflammation on bronchial homeostasis (27) .…”

Section: A Single Disease?mentioning

confidence: 99%

SCUAD and chronic rhinosinusitis. Reinforcing hypothesis driven research in difficult cases

Prokopakis¹,

Vlastos²,

Ferguson³

et al. 2014

Rhin

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The recently introduced definition of"Severe Chronic Upper Airway Disease" (SCUAD) increases awareness of those patients with persistent inflammation and symptoms despite guideline-driven pharmacologic treatment. The concept of SCUAD may prove helpful in directing research towards clarifying the definition, diagnosis and pathophysiology of rhinitis and rhinosinusitis,their limits and overlap. In this review, a hypothesis on SCUAD immunopathology is also presented.

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Section: A Single Disease?mentioning

confidence: 99%

SCUAD and chronic rhinosinusitis. Reinforcing hypothesis driven research in difficult cases

Prokopakis¹,

Vlastos²,

Ferguson³

et al. 2014

Rhin

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“…Both the nasal and bronchial mucosa are characterized by basal cells and ciliated epithelial cells in normal conditions. The histological appearance of these epithelia is similar between BA and CRS (Hellings and Prokopakis, ). NDRG1 was mainly expressed in ciliated epithelial cells in the nasal epithelium.…”

Section: Discussionmentioning

confidence: 76%

NDRG1 is important to maintain the integrity of airway epithelial barrier through claudin‐9 expression

Gon

Maruoka

Kishi

et al. 2017

Cell Biology International

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Impairment of epithelial barrier integrity caused by environmental triggers is associated with the pathogenesis of airway inflammation. Using human airway epithelial cells, we attempted to identify molecule(s) that promote airway epithelial barrier integrity. Microarray analyses were conducted using the Affimetrix human whole genome gene chip, and we identified the N-myc downstream-regulated gene 1 (NDRG1) gene, which was induced during the development of the epithelial cell barrier. Immunohistochemical analysis revealed strong NDRG1 expression in ciliated epithelial cells in nasal tissues sampled from patients with chronic rhinosinusitis (CRS), and the low expression of NDRG1 was observed in goblet cells or damaged epithelial cells. NDRG1 gene knockdown with its specific siRNA decreased the transepithelial electrical resistance and increased the dextran permeability. Immunocytochemistry revealed that NDRG1 knockdown disrupted tight junctions of airway epithelial cells. Next, we analyzed the effects of NDRG1 knockdown on the expression of tight and adhesion junction molecules. NDRG1 knockdown significantly decreased only claudin-9 expression, but did not decrease other claudin family molecules, such as E-cadherin, and ZO-1, -2, or -3. Knockdown of claudin-9 markedly impaired the barrier function in airway epithelial cells. These results suggest that NDRG1 is important for the barrier integrity in airway epithelial cells.

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“…Other pathophysiologic mechanisms than allergy seem to exist and affect the global airway disease (46). Severe forms of CRS, allergic, and non-AR have been classified recently as severe chronic upper airways disease (SCUAD) highlighting gaps in our knowledge (37,47,48).…”

Section: Discussionmentioning

confidence: 99%

Is chronic rhinosinusitis related to allergic rhinitis in adults and children? Applying epidemiological guidelines for causation

Georgalas

Vlastos

Picavet

et al. 2014

Allergy

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The relationship between allergic rhinitis and chronic rhinosinusitis has been assessed in a number of observational and experimental studies. In this review, we attempt their synthesis and evaluation using the modified Bradford Hill guidelines for causation. Although there is no proof of causation, especially in the pediatric literature, an evaluation of underlying allergies is recommended at least as an initial measure of symptoms relief.Chronic inflammatory disorders of the upper airways are extremely prevalent and have a major impact on public health (1-5). Some review articles on chronic rhinosinusitis (CRS) have suggested that atopy predisposes to its development (6), because allergic rhinitis (AR) is a common coexisting disease in pediatric and adult patients with CRS (7).Despite the fact that acute and CRS have been shown to occur frequently in AR patients, a sound pathophysiologic mechanism has not been proven, and thus, the association between rhinosinusitis and AR remains controversial (8, 9). The hallmark of AR is an IgE-mediated (type I) hypersensitivity reaction to an inciting inhaled antigen (10) and, in some cases, an ingested food that causes a cross-reaction because of antigenic similarities between the inhalant and the food (11). On the other hand, the pathophysiology of CRS is more obscure. Although the clinical presentation and symptoms of CRSwNP and CRSsNP overlap, it appears that they are underlined by distinct pathophysiological mechanisms.For example, nasal polyps (NP) have significantly higher levels of eosinophil markers, while CRSsNP is characterized by a Th1 polarization with high levels of interferon-gamma (IFN-c) and transforming growth factor-beta (TGF-b). On the other hand, CRSwNP showed a Th2 polarization with high IL-5 and immunoglobulin (Ig) E concentration (12). One step further is to assess whether the Th2 phenotype in CRSwNP is the result of the atopic status, the presence of AR, or (allergic) asthma. We know that there are many parallels between NP and asthma (13). And even some specific gene polymorphisms present in CRS have also been found in asthma (14). Several reviews on the role of allergy in CRS, in both adults (11,15) and children (16), can be found in the recent English literature, where epidemiological and experimental studies are mentioned. However, a logical structure for investigating and defining causality in epidemiological studies, such as Bradford-Hill criteria for causation, has not been Allergy 69 (2014) 828-833

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Global Airway Disease Beyond Allergy

Cited by 46 publications

References 31 publications

SCUAD and chronic rhinosinusitis. Reinforcing hypothesis driven research in difficult cases

SCUAD and chronic rhinosinusitis. Reinforcing hypothesis driven research in difficult cases

NDRG1 is important to maintain the integrity of airway epithelial barrier through claudin‐9 expression

Is chronic rhinosinusitis related to allergic rhinitis in adults and children? Applying epidemiological guidelines for causation

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