Role of Nasal Fibroblasts in Airway Remodeling of Chronic Rhinosinusitis: The Modulating Functions Reexamined

Chronic rhinosinusitis (CRS) is a multifactorial inflammatory disease of the nose and sinuses that affects more than 10% of the adult population worldwide. Currently, CRS is classified into endotypes according to the inflammatory response (Th1, Th2, and Th17) or the distribution of immune cells in the mucosa (eosinophilic and non-eosinophilic). CRS induces mucosal tissue remodeling. Extracellular matrix (ECM) accumulation, fibrin deposition, edema, immune cell infiltration, and angiogenesis are observed in the stromal region. Conversely, epithelial-to-mesenchymal transition (EMT), goblet cell hyperplasia, and increased epithelial permeability, hyperplasia, and metaplasia are found in the epithelium. Fibroblasts synthesize collagen and ECM, which create a structural skeleton of tissue and play an important role in the wound-healing process. This review discusses recent knowledge regarding the modulation of tissue remodeling by nasal fibroblasts in CRS.

Automated summary

Chronic rhinosinusitis (CRS) is a complex inflammatory disease affecting the nose and sinuses, with a prevalence of over 10% in adults globally. Different subtypes of CRS have been identified based on inflammatory response and immune cell distribution. CRS leads to tissue remodeling, characterized by extracellular matrix accumulation, immune cell infiltration, and epithelial changes. Nasal fibroblasts play a crucial role in tissue remodeling and wound healing. This review explores recent advancements in understanding the modulation of tissue remodeling by nasal fibroblasts in CRS.