Chronic Rhinosinusitis with Nasal Polyps

Stevens, Whitney W.; Schleimer, Robert P.; Kern, Robert C.

doi:10.1016/j.jaip.2016.04.012

Cited by 381 publications

(371 citation statements)

References 84 publications

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“…A recent study indicated that AhR expression in allergic nasal mucosa was increased compared to that of normal mucosa [21], but there was lower expression in the atopic CRSwNP patients [11]. AR was associated with the recurrence of CRS [22] and there was a certain correlation between AR and CRSwNP [23]. In this study, the different AhR and TGF-β1 expression levels in CRSwNPwAR (i.e., decreased AhR expression and increased TGF-β1 expression) indicated that AhR might be affected by AR and other factors; however, the detailed regulation needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

Differential Expression of the Aryl Hydrocarbon Receptor and Transforming Growth Factor Beta 1 in Chronic Rhinosinusitis with Nasal Polyps with Allergic Rhinitis

Chen

Xiao²,

Liu³

et al. 2017

ORL

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Objective: This study aimed to determine the aryl hydrocarbon receptor (AhR) and transforming growth factor beta 1 (TGF-β1) expression levels in chronic rhinosinusitis (CRS) and their possible correlation with allergic state and tissue remodeling. Methods: Patients were enrolled and divided into the following groups: CRS without nasal polyps (NP) without allergic rhinitis (AR) (CRSsNPsAR; n = 20), CRS with NP with AR (CRSwNPwAR; n = 20), CRS with NP without AR (CRSwNPsAR; n = 20), and controls (n = 15). Tissue samples were analyzed by Masson trichrome staining for collagen, while the location and expression of AhR and TGF-β1 were analyzed by immunohistochemistry, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and Western blotting. Results: The collagen amounts as well as AhR and TGF-β1 mRNA and protein expression levels were significantly increased in the CRSsNPsAR group compared with the CRSwNP (CRSwNPsAR and CRSwNPwAR) samples (p < 0.01). However, higher collagen amounts (p < 0.05) and higher TGF-β1 (p < 0.05) but lower AhR expression levels (p < 0.05) were detected in the CRSwNPwAR versus the CRSwNPsAR patients. Both AhR and TGF-β1 expression were positively correlated with the collagen level in CRS samples (p < 0.01). Conclusions: Elevated AhR expression may be involved in the progression of tissue remodeling in CRSsNPsAR similar to TGF-β1 expression. Conversely, lower AhR expression may be involved in allergic reactions in CRSwNPwAR.

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Section: Discussionmentioning

confidence: 99%

Differential Expression of the Aryl Hydrocarbon Receptor and Transforming Growth Factor Beta 1 in Chronic Rhinosinusitis with Nasal Polyps with Allergic Rhinitis

Chen

Xiao²,

Liu³

et al. 2017

ORL

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“…AERD is present in about 7% of adult asthmatics and 14% of severe asthmatics (1) and may develop in patients without a prior history of atopy, asthma or rhinitis (2). The nasal polyps of AERD patients are intensely eosinophilic and contain activated mast cells (3, 4). The disease is characterized by release of large amounts of cysteinyl leukotrienes (CysLTs) and mast cells mediators, particularly prostaglandin D2 (PGD2), after COX-1 inhibitor ingestion (5, 6).…”

Section: Introductionmentioning

confidence: 99%

Group 2 innate lymphoid cells are recruited to the nasal mucosa in patients with aspirin-exacerbated respiratory disease

Eastman

Cavagnero

DeConde

et al. 2017

Journal of Allergy and Clinical Immunology

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Background Aspirin-exacerbated respiratory disease (AERD) is characterized by tissue eosinophilia and mast cell activation, including abundant production of prostaglandin D2 (PGD2). Group 2 innate lymphoid cells (ILC2s), which promote tissue eosinophilia and mast cell responses, undergo chemotaxis and cytokine production in response to PGD2 but it is unknown whether ILC2s are active in AERD. Objective We sought to determine whether ILC2 numbers change in peripheral blood and nasal mucosa during cyclooxygenase-1 (COX-1) inhibitor-induced reactions in patients with AERD. Methods Blood and nasal scrapings were collected at baseline, during reaction, and after completion of ketorolac/aspirin challenge/desensitization in twelve patients with AERD. ILC2s and eosinophils were quantitated by flow cytometry. Urine was also collected and quantification of PGD2 metabolite and leukotriene E4 (LTE4) was done by ELISA. Baseline and NSAID-reaction clinical data was correlated with cell changes. Results ILC2s significantly increased in nasal mucosal samples and decreased in blood at the time of COX-1 inhibitor reactions in 12 patients with AERD. These changes were not observed in two patients without AERD. Further, eosinophils decreased in blood concurrently with significant increases in urinary PGD2 metabolite and LTE4. The magnitude of increases in nasal mucosal ILC2s positively correlated with maximum symptom score during the challenges. Further, the levels of blood ILC2s during the reaction correlated with the time for the reaction to resolve, possibly reflecting reaction severity. Conclusions ILC2s are recruited to the nasal mucosa during COX-1 inhibitor-induced reactions in patients with AERD, correlating with enhanced production of prostaglandins and leukotrienes.

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“…41,53 A healthy nasal epithelial barrier is known to be critical for protection against environmental factors, including allergens. 54,55 Other epithelial barrier indicators such as filaggrin (FLG), a member of the epidermal differentiation complex on chromosome 1q21, are reported to have polymorphisms and loss-of-function mutations associated with atopic dermatitis and AR. 53 It is well known that some inhaled allergens are proteinases that directly cause epithelial barrier dysfunction.…”

Section: Cell Polarization In Airway Epitheliummentioning

confidence: 99%

Airway epithelial barrier dysfunction in the pathogenesis and prognosis of respiratory tract diseases in childhood and adulthood

Yüksel

Türkeli

2017

Tissue Barriers

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The lungs are in direct contact with the environment through the tubular structure that constitutes the airway. Starting from the nasal orifice, the airway is exposed to foreign particles including infectious agents, allergens, and other substances that can damage the airways. Therefore, the airway must have a functional epithelial barrier both in the upper and lower airways to protect against these threats. As with the skin, it is likely that the pathogenesis of respiratory diseases is a consequence of epithelial barrier defects in these airways. The characteristics of this system, starting from the beginning of life and extending into maturing and aging, determine the prognosis of respiratory diseases. In this article, we discuss the pathogenesis, clinical phenotype, and prognosis of respiratory diseases from newborns to adulthood in the context of epithelial barrier function and dysfunction.

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Chronic Rhinosinusitis with Nasal Polyps

Cited by 381 publications

References 84 publications

Differential Expression of the Aryl Hydrocarbon Receptor and Transforming Growth Factor Beta 1 in Chronic Rhinosinusitis with Nasal Polyps with Allergic Rhinitis

Differential Expression of the Aryl Hydrocarbon Receptor and Transforming Growth Factor Beta 1 in Chronic Rhinosinusitis with Nasal Polyps with Allergic Rhinitis

Group 2 innate lymphoid cells are recruited to the nasal mucosa in patients with aspirin-exacerbated respiratory disease

Airway epithelial barrier dysfunction in the pathogenesis and prognosis of respiratory tract diseases in childhood and adulthood

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