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Activation Of Pyroptosis Impairs Basal Cell Differentiation In The Nasal Epithelium In Chronic Rhinosinusitis With Nasal Polyps.

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Activation Of Pyroptosis Impairs Basal Cell Differentiation In The Nasal Epithelium In Chronic Rhinosinusitis With Nasal Polyps.

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Activation of pyroptosis impairs basal cell differentiation in the nasal epithelium in chronic rhinosinusitis with

Guangmin Zhang¹, Shengxi Jin², Jiane Liu²

¹Department of Otolaryngology, Head and Neck Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, P.R. China.

Molecular Medicine Reports

|June 13, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Pyroptosis, a cell death process, drives chronic rhinosinusitis with nasal polyps (CRSwNP) by disrupting nasal epithelial cell differentiation. Targeting pyroptosis may offer new therapeutic strategies for CRSwNP.

Keywords:

basal cell differentiation chronic rhinosinusitis with nasal polyps nasal epithelium pyroptosis

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Area of Science:

Immunology
Cell Biology
Otorhinolaryngology

Background:

Chronic rhinosinusitis with nasal polyps (CRSwNP) affects 2-4% of the population and is characterized by chronic inflammation.
Pyroptosis, a pro-inflammatory programmed cell death, is implicated in CRSwNP pathogenesis, but its precise role and molecular drivers are not fully understood.

Purpose of the Study:

To investigate the role of pyroptosis in CRSwNP pathogenesis.
To identify molecular mechanisms and potential therapeutic targets for CRSwNP.

Main Methods:

Analysis of nasal tissue from CRSwNP patients (eosinophilic and non-eosinophilic subtypes) using HE, IHC, and IF staining for pyroptosis markers (NLRP3, IL-1β, GSDMD, Caspase-1).
In vitro studies using primary human nasal epithelial cells (HNEpCs) with Western blotting, RT-qPCR, and RNA-sequencing.

Serum analysis to identify pyroptosis triggers.

Main Results:

Elevated pyroptosis markers (NLRP3, IL-1β) were observed in CRSwNP tissues, with higher levels in non-ECRSwNP compared to ECRSwNP.
IL-5 and IL-17A were identified as key pyroptosis triggers in ECRSwNP and nECRSwNP, respectively.
Pyroptosis activation led to disrupted basal cell differentiation and promoted goblet cell differentiation, a hallmark of CRSwNP. Inhibition of pyroptosis restored basal cell differentiation and suppressed inflammation.

Conclusions:

Pyroptosis is a significant pathological driver in CRSwNP.
Targeting pyroptosis presents a promising therapeutic avenue for restoring epithelial homeostasis and managing CRSwNP symptoms.