Akademik Veri Yönetim Sistemi
World Immune Regulation Meeting XVIII 2024, Chur, İsviçre, 13 - 16 Mart 2024, cilt.18, sa.49, ss.65
Air pollution is responsible for an estimated 3.7 to 4.2 million annual deaths worldwide, with associations with the onset and exacerbation of respiratory diseases such as asthma and chronic obstructive pulmonary diseases. We investigated the synergistic effect between various air pollutants in the presence or absence of type 1 and type 2 inflammation. For epithelial cell culture, a 3D culture model, nasal epithelial spheroids (NES) were used. NES were treated with various cytokines such as IL-13 and IFN-γ to mimic different types 1 and 2 inflammatory responses and exposed to diesel exhaust particles, formaldehyde and acetaldehyde for 2 days. IL-13 treatment caused epithelial barrier impairment at 30 ng/ml, as demonstrated by paracellular flux assay. mRNA levels of the goblet cell marker (MUC5AC) showed a substantial increase, while cilia cell markers (DNAI2, FOXJ1) and club cell marker (SCGB1A1) were decreased. In addition, mRNA levels of the antimicrobial peptide BPIFA1 were also notably diminished. IFN-γ treatment caused epithelial barrier impairment at 60 ng/ml. mRNA levels of basal cell (ITGA6) was increased and cilia cell (DNAI2) was decreased. Formaldehyde, acetaldehyde and diesel exhaust caused exhibited deleterious effects on the epithelial barrier at the same concentration of 104 μg/m3. Overall, we established in vitro models of nasal type 1 and type 2 inflammation and air pollution exposure models with NES. The air pollutants in daily exposed doses and cytokines such as IL-13 and IFN-y that can be found in inflammatory tissues cause barrier impairment.