Abstract
BackgroundIn airway epithelium, thymus and activation-regulated chemokine (CCL17) and macrophage-derived chemokine (CCL22) are induced by defective epithelial barriers such as E-cadherin and attract the effector cells of Th2 immunity. However, the association between the epithelial barrier and CCL17 expression has not been studied in chronic rhinosinusitis with nasal polyp (CRSwNP). Thus, we aimed to evaluate the expression of CCL17 and its regulation by Th cytokines in nasal polyp (NP) epithelial cells.MethodsThe expression and distribution of CCL17, CCL22, E-cadherin and/or epidermal growth factor receptor (EGFR) were measured using real-time PCR, western blot, and immunohistochemistry and compared between normal ethmoid sinus epithelium and NP epithelium. In addition, the expression level of CCL17 was determined in cultured epithelial cells treated with IL-4, IL-5, IL-13, TNF-α, and IFN-γ.ResultsThe expression of CCL17 was decreased in the NP epithelium compared to the epithelium of normal ethmoid sinus, whereas the expression of CCL22 was not decreased. E-cadherin was differentially distributed between the epithelium of normal ethmoid sinus and NP epithelium. EGFR was also decreased in NPs. Interestingly, the stimulation of cultured epithelial cells with Th2 cytokines, IL-4 and IL-5, resulted in an upregulation of CCL17 expression only in NP epithelial cells whereas the expression of CCL17 was increased in both normal epithelial cells and NP epithelial cells by Th1 cytokines.ConclusionOur results suggest that the decreased expression of CCL17 in defective NP epithelium may be closely connected to NP pathogenesis and can be differentially regulated by cytokines in the NP epithelium of patients with CRSwNP.
Highlights
Chronic rhinosinusitis (CRS) is a chronic and persistent inflammatory disease of the sinonasal mucosa
The expression of CCL17 was decreased in the nasal polyp (NP) epithelium compared to the epithelium of normal ethmoid sinus, whereas the expression of CCL22 was not decreased
CCL17 expression was decreased in NP epithelium
Summary
Chronic rhinosinusitis (CRS) is a chronic and persistent inflammatory disease of the sinonasal mucosa. A nasal polyp (NP) is a mucosal sac containing edema, fibrous tissue, vessels, inflammatory cells, and glands with disrupted epithelium.[1] NPs frequently accompany CRS, and their presence complicates the treatment of this disease.[2] CRS with NP (CRSwNP) in Asian patients predominantly show a mixed T cell immune response whereas CRSwNP in Western patients is typically characterized by Th2 cytokine polarization.[3, 4] the mechanisms that induce the Th2 response seem integral to the pathogenesis of CRSwNP, these mechanisms are not fully understood in Asian patients.[5]. We aimed to evaluate the expression of CCL17 and its regulation by Th cytokines in nasal polyp (NP) epithelial cells
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