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The effect of urban particulate matter on cultured human nasal fibroblasts
Author(s) -
Lee Dong Chang,
Choi Hyunsu,
Oh JeongMin,
Hong Yupyo,
Jeong Su Hee,
Kim Choung Soo,
Kim DongKee,
Cho WonKyung,
Kim Sung Won,
Kim Soo Whan,
Cho Jin Hee,
Lee Joohyung
Publication year - 2018
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.22167
Subject(s) - medicine , tumor necrosis factor alpha , p38 mitogen activated protein kinases , chemokine , respiratory tract , fibroblast , signal transduction , cytokine , phosphorylation , viability assay , blot , messenger rna , transcription factor , immunology , inflammation , microbiology and biotechnology , respiratory system , protein kinase a , biology , cell , biochemistry , gene , in vitro
Background Exposure to urban particulate matter (UPM) has been linked to aggravation of various health problems. Although the effects of UPM on the lower respiratory tract have been extensively studied, more research is required on the impact of UPM on the upper respiratory tract and the underlying mechanisms. Thus, we investigated the cytotoxic effects of UPM on cultured human nasal fibroblasts, the underlying signaling pathways involved, and changes in cytokine levels. Methods Human turbinate tissue specimens were collected during partial turbinectomies performed on 6 patients, and then cultured. The effect of UPM on nasal fibroblast viability was explored. Real‐time reverse transcription‐polymerase chain reaction was used to measure the mRNA levels of genes encoding cytokines and chemokines (interleukin [IL]‐4, IL‐6, IL‐8, and tumor necrosis factor‐α) before and after 24 hours of UPM treatment. Enzyme‐linked immunosorbent assays were employed to measure IL‐6 and IL‐8 levels. The status of the p38 and nuclear factor (NF)‐κB signaling pathways was analyzed by Western blotting. Results UPM reduced cell viability in a dose‐dependent manner and increased IL‐6 and IL‐8 expression at both the mRNA and protein levels. UPM induced the phosphorylation of p38 and NF‐κB p65; inhibitors of the actions of these proteins repressed phosphorylation and the expression of IL‐6 and IL‐8. Conclusion UPM induced IL‐6 and IL‐8 expression by fibroblasts via p38 and NF‐κB classical signaling, suggesting that UPM can induce or aggravate allergic and/or chronic rhinitis.