Distinct expression of NK2 homeobox 1 (NKX2‐1) and goblet cell hyperplasia in nasal polyps with different endotypes

Du, Jing; Ba, Luo; Li, Bo; Liu, Feng; Hu, Xianting; Zhang, Jie; Liu, Yafeng; Xian, Jing; Liu, Sixi; Li, Hua-Bin

doi:10.1002/alr.21932

Cited by 8 publications

(7 citation statements)

References 24 publications

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“…Although it is known that Th2 inflammation induces goblet cell hyperplasia in the lung and in nasal polyps, our group did not find any change in MUC5AC expression (a specific marker for airway goblet cells) in AR nor in CRSwNP, while other studies showed opposing findings . Recently, goblet cell hyperplasia has been shown to be specifically present in IL‐5 high NP, and therefore, it might be a specific feature of severe CRSwNP with a strong Th2 profile. An increased number of basal cells have been described in CRSwNP, possibly reflecting reduced differentiation into ciliated cells.…”

Section: Epithelial Dysfunction In the Diseased Epitheliumcontrasting

confidence: 86%

“…Mucociliary function has been described to be impaired in CRSsNP and CRSwNP, partially due to epithelial de‐differentiation (via EMT) in addition to changes in cells specification (ie changes in the proportion of basal, ciliated or goblet cells) . Recently, it has been demonstrated that primary NECs derived from nasal basal cells isolated from NP show an abnormal cilia architecture with a decreased beat frequency compared with healthy controls …”

Section: Epithelial Dysfunction In the Diseased Epitheliummentioning

confidence: 99%

“…In pathological conditions, alterations in glycosylation of these mucins can lead to an increased mucus viscosity, which contributes to airway obstruction . As mentioned above, studies are conflicting about the expression of MUC5AC and MUC5B in patients with CRSwNP with either a reported increase or a decrease of these mucins . This could be explained by the fact that MUC5A has been suggested to be produced only by a distinct subset of secretory goblet cells .…”

Section: Epithelial Dysfunction In the Diseased Epitheliummentioning

confidence: 99%

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Key role of the epithelium in chronic upper airways diseases

Gohy

Hupin

Ladjemi

et al. 2019

Clin Experimental Allergy

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The respiratory epithelium of the upper airways is a first‐line defence against inhaled irritants, pathogens and allergens. It ensures a physical barrier provided by apical junctions and mucociliary clearance to avoid excessive activation of the immune system. The epithelium also forms a chemical and immunological barrier, extensively equipped to protect the airways against external aggressions before the adaptive immune system is required. Under normal circumstances, the epithelium is capable of recovering rapidly after damage. This manuscript reviews these main properties of the upper airway epithelium as well as its reported impairments in chronic inflammatory diseases. The knowledge on normal epithelial functions and their dysregulation in upper airway diseases should help to design new epithelial‐targeted treatments.

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Section: Epithelial Dysfunction In the Diseased Epitheliumcontrasting

confidence: 86%

Section: Epithelial Dysfunction In the Diseased Epitheliummentioning

confidence: 99%

Section: Epithelial Dysfunction In the Diseased Epitheliummentioning

confidence: 99%

See 1 more Smart Citation

Key role of the epithelium in chronic upper airways diseases

Gohy

Hupin

Ladjemi

et al. 2019

Clin Experimental Allergy

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“…However, studies suggest that STAT3 transcription factors can act as transcriptional repressors by interfering with other transcription factors ( de la Iglesia et al, 2008 ; Bedel et al, 2011 ). Meanwhile other studies indicated that transcription factor SPDEF was an upstream regulator for FOXA2 expression ( Yu et al, 2010 ; Du et al, 2017 ). We found no significantly different changes in the expression of SPDEF after curcumin treatment of NCI-H292 cells (data not shown), suggesting SPDEF might not be involved in curcumin-mediated FOXA2 expression.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Inhibits Growth of Human NCI-H292 Lung Squamous Cell Carcinoma Cells by Increasing FOXA2 Expression

et al. 2018

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Lung squamous cell carcinoma (LSCC) is a common histological lung cancer subtype, but unlike lung adenocarcinoma, limited therapeutic options are available for treatment. Curcumin, a natural compound, may have anticancer effects in various cancer cells, but how it may be used to treat LSCC has not been well studied. Here, we applied curcumin to a human NCI-H292 LSCC cell line to test anticancer effects and explored underlying potential mechanisms of action. Curcumin treatment inhibited NCI-H292 cell growth and increased FOXA2 expression in a time-dependent manner. FOXA2 expression was decreased in LSCC tissues compared with adjacent normal tissues and knockdown of FOXA2 increased NCI-H292 cells proliferation. Inhibition of cell proliferation by curcumin was attenuated by FOXA2 knockdown. Moreover inhibition of STAT3 pathways by curcumin increased FOXA2 expression in NCI-H292 cells whereas a STAT3 activator (IL-6) significantly inhibited curcumin-induced FOXA2 expression. Also, SOCS1 and SOCS3, negative regulators of STAT3 activity, were upregulated by curcumin treatment. Thus, curcumin inhibited human NCI-H292 cells growth by increasing FOXA2 expression via regulation of STAT3 signaling pathways.

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“…An increase in goblet cell accumulation has been noted in chronic allergic airway disease as well as mouse models of chronic sinonasal inflammation. 25,26 A recent study reported increased goblet cell hyperplasia in human nasal epithelial cultures treated with IL-33 in vitro. 27 Thus, the exaggerated increase of goblet cells in Nrf2 −/− mice may be in response to the elevated expression of IL-33 (Fig.…”

Section: Discussionmentioning

confidence: 99%

Deletion of Nrf2 enhances susceptibility to eosinophilic sinonasal inflammation in a murine model of rhinosinusitis

London

Tharakan

Mendiola³

et al. 2018

Int Forum Allergy Rhinol

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Background: Oxidative stress exacerbates lower airway diseases including asthma and chronic obstructive pulmonary disease (COPD); however, its role in upper airway (sinonasal) chronic inflammatory disorders is less clear. Nuclear erythroid 2 p45-related factor (Nrf2) is an endogenous mechanism that upon activation invokes an antioxidant response pathway via nuclear translocation and upregulation of cytoprotective genes. We sought to determine whether deletion of Nrf2 enhances susceptibility to allergic sinonasal inflammation in vivo. Methods: Nrf2−/− mice were subjected to the ovalbumin (Ova)-induced murine model of rhinosinusitis and indices of sinonasal inflammation and epithelial barrier dysfunction were assessed. Results: We show that deletion of Nrf2 results in enhances indices of allergen-induced sinonasal inflammation including aggravated eosinophil accumulation and goblet cell hyperplasia. An exaggerated increase in epithelial derived inflammatory cytokines including interleukin 33 (IL-33) and thymic stromal lymphopoietin (TSLP) was observed in the nasal lavage fluid and sinonasal mucosal tissue of Nrf2−/− mice. Furthermore, Nrf2−/− mice showed heightened Ova-induced barrier dysfunction as measured by serum albumin accumulation in nasal lavage fluid of mice. Conclusion: These data show that the endogenous Nrf2 pathway limits Ova-induced sinonasal inflammation, epithelial derived inflammatory cytokine production, and epithelial barrier dysfunction in vivo and identify a potential therapeutic target in the management of allergic sinonasal inflammatory disorders. This is the first study to our knowledge which shows that Nrf2 regulates allergic inflammation in the sinonasal cavity in vivo.

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Distinct expression of NK2 homeobox 1 (NKX2‐1) and goblet cell hyperplasia in nasal polyps with different endotypes

Abstract: The downregulation of NKX2-1 in IL-5 NPs may be associated with tissue eosinophilia and goblet cells hyperplasia.

Cited by 8 publications

References 24 publications

Key role of the epithelium in chronic upper airways diseases

Key role of the epithelium in chronic upper airways diseases

Curcumin Inhibits Growth of Human NCI-H292 Lung Squamous Cell Carcinoma Cells by Increasing FOXA2 Expression

Deletion of Nrf2 enhances susceptibility to eosinophilic sinonasal inflammation in a murine model of rhinosinusitis

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