Epithelial-to-mesenchymal transition in neutrophilic chronic rhinosinusitis. Issue 1 (February 2021)

• Record Type: Journal Article
• Authors: Ryu, Gwanghui; Mo, Ji-Hun; Shin, Hyun-Woo
• Is Part Of: Current opinion in allergy and clinical immunology. Volume 21:Issue 1(2021)
• Publication Date: 2021-02
• Subjects: epithelial-to-mesenchymal transition -- interferon-γ -- nasal polyp -- neutrophil -- rhinosinusitis; Allergy -- Periodicals; Clinical immunology -- Periodicals; Hypersensitivity; Immunity; Immune System Diseases; Allergy and Immunology; 616.079
• DOI: 10.1097/ACI.0000000000000701
• Languages: English
• ISSNs: 1528-4050

Abstract

Abstract : Purpose of review: Barrier dysfunction, tissue fibrosis, and remodeling are essential processes of the pathophysiology of chronic rhinosinusitis (CRS). The role of epithelial-to-mesenchymal transition (EMT) has been assessed in various studies in CRS. In this review, we summarized the pathophysiologic mechanisms of EMT related to CRS, particularly neutrophilic CRS. Recent findings: Loss of epithelial characteristics due to EMT makes leaky epithelium, and transformed mesenchymal cells cause fibrosis and remodeling. Hypoxia, allergens (house dust mites), infections, and air pollutants were related to the pathogenesis of neutrophilic CRS, and these factors are known to induce barrier dysfunction and EMT in sinonasal epithelia. Some molecular pathways related to EMT have been recognized in CRS, including interferon-γ/p38/extracellular signal-regulated kinase, high-mobility group box 1/receptor of advanced glycosylation end-products, TGF-β1/SMAD, and Wnt/β-catenin-signaling pathways. Apart from, several microRNAs (miR-21, miR-761, and miR-30a-5p) have been identified to regulate EMT in CRS. Summary: EMT is considered to be an important pathogenesis mechanism for CRS. The factors cause EMT in CRS, and the associated molecular mechanisms are related to neutrophilic inflammation. Further studies on CRS endotype and/or phenotype are needed to clarify the implication of EMT on CRS pathogenesis.