Differential short palate, lung, and nasal epithelial clone 1 suppression in eosinophilic and noneosinophilic chronic rhinosinusitis with nasal polyps

Wei, Yi; Han, Miaomiao; Wen, Wang; Li, Hua-Bin

doi:10.1097/aci.0000000000000228

Cited by 6 publications

(6 citation statements)

References 85 publications

(91 reference statements)

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“…Better understanding of the role of BPIFA1 in disease pathogenesis will elucidate its potential as a biomarker and potential drug target against pulmonary disease. Nasal SPLUNC1 expression is inhibited by Th2 cytokines (IL-4 and IL-13) [35,36] but stimulated by Toll-like receptor (TLR) agonists and glucocorticoids [37].…”

Section: Database Analysismentioning

confidence: 99%

Bioinformatics Analysis and Identification of Underlying Biomarkers Potentially Linking Allergic Rhinitis and Asthma

et al. 2020

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Background:Rhinitis is the most common clinical manifestation of allergy, affecting more than 400 million people around the world. Rhinitis increases the risk of developing bronchial hyper-responsiveness and asthma. Previous studies have shown that rhinitis is closely related with the physiology, pathology, and pathogenesis of asthma. We analyzed co-expressed genes to explore the relationships between rhinitis and asthma and to find biomarkers of comorbid rhinitis and asthma. Material/Methods:Asthma-and rhinitis-related differentially-expressed genes (DEGs) were identified by bioinformatic analysis of GSE104468 and GSE46171 datasets from the Gene Expression Omnibus (GEO) database. After assessment of Gene Ontology (GO) terms and pathway enrichment for DEGs, a protein-protein interaction (PPI) network was conducted via comprehensive target prediction and network analyses. We also evaluated co-expressed DEGs and corresponding predicted miRNAs involved in the developing process of rhinitis and asthma. Results:We identified 687 and 1001 DEGs in bronchial and nasal epithelia samples of asthma patients, respectively. For patients with rhinitis, we found 245 DEGs. The hub-genes of PAX6, NMU, NTS, NMUR1, PMCH, and KRT6A may be associated with rhinitis, while CPA3, CTSG, POSTN, CLCA1, HDC, and MUC5B may be involved in asthma.The co-expressed DEGs of BPIFA1, CCL26, CPA3, and CST1, together with corresponding predicted miRNAs (e.g., miR-195-5p and miR-125a-3p) were found to be significantly correlated with rhinitis and asthma. Conclusions:Rhinitis and asthma are related, and there are significant correlations of BPIFA1, CCL26, CPA3, and CST1 genes with novel biomarkers involved in the comorbidity of rhinitis and asthma.

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Section: Database Analysismentioning

confidence: 99%

Bioinformatics Analysis and Identification of Underlying Biomarkers Potentially Linking Allergic Rhinitis and Asthma

et al. 2020

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“…The majority of the available studies are based on the histological analysis of nasal polyps, while experiences on CRSwNP and nasal cytology are limited, but in line with the previous literature. In fact, Gelardi et al studied the presence of the inflammatory cell population in the nasal mucosa of patients with CRSwNP and without allergy, demonstrating that the most represented cell types were eosinophils (61.8%), associated with mast cells in a further 31.9% of patients. Furthermore, they showed the mast cells/eosinophils association was more frequently associated to a clinical phenotype, namely patients with polyposis, asthma and ASA‐sensitivity …”

Section: Chronic Rhinusinusitis With and Without Nasal Polypsmentioning

confidence: 99%

Nasal cytology: Methodology with application to clinical practice and research

Heffler

Landi

Caruso

et al. 2018

Clin Experimental Allergy

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Nasal cytology is an easy, cheap, non-invasive and point-of-care method to assess nasal inflammation and disease-specific cellular features. By means of nasal cytology, it is possible to distinguish between different inflammatory patterns that are typically associated with specific diseases (ie, allergic and non-allergic rhinitis). Its use is particularly relevant when other clinical information, such as signs, symptoms, time-course and allergic sensitizations, is not enough to recognize which of the different rhinitis phenotypes is involved; for example, it is only by means of nasal cytology that it is possible to distinguish, among the non-allergic rhinitis, those characterized by eosinophilic (NARES), mast cellular (NARMA), mixed eosinophilic-mast cellular (NARESMA) or neutrophilic (NARNE) inflammation. Despite its clinical usefulness, cheapness, non-invasiveness and easiness, nasal cytology is still underused and this is at least partially due to the fact that, as far as now, there is not a consensus or an official recommendation on its methodological issues. We here review the scientific literature about nasal cytology, giving recommendations on how to perform and interpret nasal cytology.

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“…Studied examples in CRS include epithelial-derived proteins, such as defensins, cathelicidins, lysozyme, and SPLUNC1. 20,[28][29][30] As an example, Wei et al recently showed that SPLUNC1 is suppressed in eosinophilic CRSwNP when compared with noneosinophilic CRSwNP and that its expression can be decreased by stimulation with Th2 cytokines IL-4 and IL-13. 29 At present, the drivers of the exaggerated type 2 inflammatory response and fungal overgrowth in AFRS are unclear; however, loss of antimicrobial defense peptides (eg, histatin) may support fungal/antimicrobial growth and promote a skewed Th2 immune profile, such as the one observed in AFRS.…”

Section: Discussionmentioning

confidence: 99%

Distinguishing Molecular Features of Allergic Fungal Rhinosinusitis

Tyler

Dietz

Citardi

et al. 2018

Otolaryngol.--head neck surg.

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Objective Allergic fungal rhinosinusitis (AFRS) is a clinical subtype of chronic rhinosinusitis with nasal polyps (CRSwNP), characterized by eosinophilic mucin, evidence of fungal elements within the mucin, fungal-specific type I hypersensitivity, and characteristic computed tomography findings. It remains controversial whether AFRS represents a disease with a unique pathophysiology from chronic rhinosinusitis or is merely a severe form of CRSwNP. The goal of this study was to identify molecular features unique to AFRS. Study Design Cross-sectional case-control. Setting Single academic tertiary referral institution. Subjects and Methods Subjects included 86 patients undergoing endoscopic sinus surgery: CRSwNP (n = 34), AFRS (n = 37), and healthy controls (n = 15). Pathway and correlation analyses were performed with whole-genome microarray data for study patients undergoing surgery for recalcitrant chronic rhinosinusitis. Our findings were confirmed with quantitative polymerase chain reaction and immunohistochemical studies. Results AFRS was uniquely characterized by a pronounced association with adaptive T helper 2-associated immune gene expression. AFRS exhibited altered expression of proteins associated with secretory salivary peptides-namely, histatin, a peptide with known antifungal activity in the oral cavity. Furthermore, the expression of histatins correlated negatively with that of type 2 inflammatory mediators. We confirm the decreased expression of histatins in AFRS when compared with CRSwNP by quantitative polymerase chain reaction and localized its expression to a submucosal cell population. Conclusion There exist clear molecular profiles that distinguish AFRS from CRSwNP. This divergence translates into an altered ability to control fungal growth and may in part explain some of the phenotypical differences between CRSwNP and AFRS.

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Differential short palate, lung, and nasal epithelial clone 1 suppression in eosinophilic and noneosinophilic chronic rhinosinusitis with nasal polyps

Cited by 6 publications

References 85 publications

Bioinformatics Analysis and Identification of Underlying Biomarkers Potentially Linking Allergic Rhinitis and Asthma

Bioinformatics Analysis and Identification of Underlying Biomarkers Potentially Linking Allergic Rhinitis and Asthma

Nasal cytology: Methodology with application to clinical practice and research

Distinguishing Molecular Features of Allergic Fungal Rhinosinusitis

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