ADAM28 promotes epithelial mesenchymal transition and impairs tight junctions in non-eosinophilic chronic rhinosinusitis with nasal polyps by inducing M1 polarization of macrophages.

Background: Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by tight junction dysfunction associated with epithelial-mesenchymal transition (EMT) processing. ADAM28 participates in the pathogenic process of inflammatory airway diseases.

Methods: The effects of ADAM28 knockdown on the expression levels of the M1-type macrophage markers were examined using M1-type macrophage polarization model established with the THP1 cells.

Signaling lymphocytic activation molecule family 8 disrupts epithelial barrier in chronic rhinosinusitis with nasal polyps through M1 macrophage polarization.

Background: Recent studies reveal that M1 macrophages accumulate predominantly in noneosinophilic chronic rhinosinusitis with nasal polyps (neCRSwNP). However, the precise mechanisms regulating M1 macrophages and their impact on the epithelial barrier remain unclear.

Objective: To investigate the expression and regulatory role of signaling lymphocytic activation molecule family (SLAMF)8, a molecule exclusively expressed in myeloid cells, in M1 macrophage polarization and its potential contribution to neCRSwNP development.

Clinical Significance of HMGB1 and Autophagy-Related Genes in Sinonasal Inverted Papilloma.

Objectives: Sinonasal inverted papilloma (SNIP) is a noncancerous tumor that develops in the mucous membrane of the nasal sinuses. Many malignancies are tightly linked to autophagy, an intracellular self-degradation mechanism. HMGB1 has demonstrated its ability to modulate autophagy in many pathological conditions.

Identification of Pyroptosis-Related Genes Regulating the Progression of Chronic Rhinosinusitis with Nasal Polyps.

Introduction: Chronic rhinosinusitis with nasal polyps (CRSwNP) is an immunologic disease, and pyroptosis, an inflammation-based cellular death, strictly modulates CRSwNP pathology, whereas the pyroptosis genes and mechanisms involved in CRSwNP remain unclear. Herein, we explored disease biomarkers and potential therapeutic targets for pyroptosis and immune regulation in CRSwNP using bioinformatics analysis and tissue-based verification.

Methods: We retrieved the transcriptional profiles of the high-throughput dataset GSE136825 from the Gene Expression Omnibus database, as well as 170 pyroptosis-related gene expressions from GeneCards.

Reduced Proliferative Capacity and Defense against Staphylococcus aureus in Human Nasal Mucosal Epithelium Lacking ZNF365.

Introduction: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a common chronic inflammatory disease of the nose characterized by barrier disruption and environmental susceptibility, and the deletion of ZNF365 may be a factor inducing these manifestations. However, there is no study on the mechanism of action between CRSwNP and ZNF365. Therefore, this study focuses on the effect of the zinc finger protein ZNF365 on the proliferation of nasal mucosal epithelial cells and their defense against Staphylococcus aureus (S.