Effect of fluticasone propionate on human nasal fibroblasts exposed to urban particulate matter. Issue 3 (June 2020)

• Record Type: Journal Article
• Authors: Kim, Ji-Sun; Choi, Hyunsu; Oh, Jeong-Min; Kim, Yoon-Ho; Kim, Sung Won; Kim, Soo Whan; Kim, Byung Guk; Cho, Jin Hee; Lee, Joohyung; Lee, Dong Chang
• Is Part Of: Auris nasus larynx. Volume 47:Issue 3(2020)
• Page Start: 415
• Page End: 424
• Publication Date: 2020-06
• Subjects: Fluticasone -- Particulate matter -- Fibroblast -- Interleukin-6 -- CXC chemokine ligand (CXCL)1; Otolaryngology -- Periodicals; Electronic journals; 616
• DOI: 10.1016/j.anl.2019.11.002
• Languages: English
• ISSNs: 0385-8146

Abstract

Abstract: Objective: Particulate matter (PM), which contains organic compounds and toxic metals, is the major cause of air pollution. PM enters the body, causing various health problems. Although the effects of PM on the lower respiratory tract have been extensively investigated, the effects on the upper respiratory tract (including the nasal cavity) require further evaluation. To investigate the effect of fluticasone propionate (FP) on nasal fibroblasts exposed to UPM. Methods: Samples of inferior turbinate tissue were obtained from six patients. The fibroblasts isolated from these samples were exposed to UPM and/or FP. The expression of interleukin (IL)-6, CXC chemokine ligand (CXCL) 1, IL-1β, and tumour necrosis factor-alpha (TNF-α) in nasal fibroblasts was analysed using real-time PCR and enzyme-linked immunosorbent assays. The protein levels of nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) were analysed by western blotting. Results: FP reversed the UPM-induced reduction in cell viability. The mRNA and protein levels of IL-6, CXCL1, IL-1β, and TNF-α were significantly increased by UPM. FP reversed the UPM-induced increases in the protein levels of NF-κB and phosphorylated-STAT3 in a dose-dependent manner. In addition, TNF-α, an inducer of NF-κB, reversed the FP-induced reduction in the levels of signalling molecules. Conclusion: UPM induces the expression of IL-6, CXCL1, IL-1β, and TNF-α in nasal fibroblasts and this effect is reversed by FP via the STAT3 and NF-κB signalling pathways. These results suggest that FP has therapeutic potential for nasal diseases related to UPM, such as allergic and chronic rhinitis.