Abstract
Chronic rhinosinusitis is a common inflammatory disease of paranasal sinuses, which causes rhinorrhea, nasal congestion, and hyposmia. The genetic predisposition or the exposure to irritants can sustain the inflammatory response and the development of nasal polyposis. Nasal polyps are benign and teardrop-shaped growths that project in the nasal cavities, and originate from the ethmoid sinuses. This inflammatory process is associated with high expression of IL-4, IL-5 and IL-13 and IgE. Antibodies targeting these cytokines or receptors represent a therapeutic strategy in the treatment of nasal polyposis in combination with corticosteroids. The molecular pathogenesis of nasal polyps in chronic rhinosinusitis (CRS) patients is associated with remodeling transition, a process in which epithelial cells lose their typical phenotype, acquiring a mesenchymal-like aspect. TGFβ/SMAD, ERK, and Wnt/β-catenin pathways are altered during the nasal tissue remodeling. miRNA and inhibitor molecules targeting these signaling pathways are able to interfere with the process; which could lead to alternative therapies. Nasal polyps are an alternative source of mesenchymal stem cells, which can be isolated from surgical biopsies. A molecular understanding of the biology of PO-MSCs will contribute to the delineating inflammatory process underlying the development of nasal polyps.
Highlights
Recent studies have demonstrated a role for miR-21 in mediating TGF-β1-induced Epithelial mesenchymal transition (EMT) in primary human nasal epithelial cells via the PTEN/Akt pathway during the pathogenesis of CRS with nasal polyps (CRSwNP) [38]. miR-21 inhibitors could be considered as anti-polyp drugs for treating nasal polyps [38] as well as recent findings that suggest glucocorticoids might prevent tissue remodeling by blocking the EMT initiated by TGF-β1-induced mitogen-activated protein kinase (MAPK) and Snail/Slug signaling pathways in CRSwNP [38,39]
Studies have demonstrated that the AGE/receptor of advanced glycosylation end products (RAGE)/ERK pathway is involved in the pathogenesis of CRSwNP promoting EMT and tissue remodeling
Chronic rhinosinusitis with nasal polyps (CRSwNP) is one of the most common respiratory diseases worldwide. This disorder affects over ten percent of the adult population and the prevalence increases with age, causing a significant reduction in patients’ quality of life
Summary
The nasal disorder of CRS is a chronic condition of the upper airway characterized histologically by the infiltration of inflammatory cells like eosinophils or neutrophils of the paranasal sinuses and nasal cavity [1,2] affecting 5–12% of the population. Nasal polyps (NP) derived from the middle meatus are inflammatory outgrowths of paranasal sinus mucosa, most often benign, frequently bilateral, and typically develop in adulthood, and are characterized by inflammation [3,4]. They present an abnormal remodeling response and a lack of immunoregulation, creating an imbalance and, favoring inflammation. With localized primary CRS, which are usually unilateral or bilateral in distribution, those with typically inflammatory endotype dominance are separated into a type 2 skewed inflammation and can be exacerbated in allergic fungal rhinosinusitis (AFRS, ) while non-type 2 disease is found in isolated sinusitis. The secondary CRS involves a wide range of clinical phenotypes including fungal ball, tumors, primary ciliary dyskinesia, cystic fibrosis, granulomatosis with polyangiitis (GPA) (Wegener’s disease), and eosinophilic granulomatosis with polyangiitis (EGPA) (Churg-Strauss disease) with different immunodeficiency’s [1,3]
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