한빛사논문
Nahyun Kim PhD1,¶, Dohyun Han PhD2,¶, Injae Joseph Wang MS2, Doo Hee Han MD, PhD3, Myung-Whan Suh MD, PhD3,4, Jun Ho Lee MD, PhD3,4, Seung-Ha Oh MD, PhD3,4, Moo Kyun Park MD, PhD3,4,*
1Center for Medical Innovation, Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
2Proteomics Core Facility, Biomedical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
3Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Republic of Korea
4Sensory Organ Research Institute, Seoul National University Medical Research Center, Seoul, Republic of Korea
¶These authors contributed equally to this work. All authors have no conflicts to disclose.
*Corresponding author.
Abstract
Background
Airway epithelial cells can actively participate in the defense against environmental pathogens to elicit local or systemic inflammation. Diesel exhaust particles (DEPs), a main component of urban air pollution with particulate matter (PM), are associated with the occurrence of acute and chronic upper airway inflammatory diseases.
Objectives
We sought to investigate the effect of DEPs alone or in combination with lipopolysaccharide (LPS) on the secretome in the primary human nasal epithelium (PHNE) and to find potential biomarkers to relate DEP exposure to upper airway inflammatory diseases.
Methods
PHNE were cultured at an air–liquid interface to create a differentiated in vivo-like model. Secreted proteins (secretome) on the bottom media of the PHNE were analyzed using mass spectrometry–based label-free quantitative proteomics and ELISA.
Results
Considerably more differentially expressed secreted proteins were identified in response to DEPs plus LPS than to DEPs alone. Some canonical pathways related to inflammation and cancer such as the p53, β-catenin and ERK1/2 pathways were involved. Among differentially expressed secreted proteins, leukemia inhibitory factor (LIF) was also detected at a high level in the middle ear effusions (MEEs) of otitis media (OM) patients, and the LIF level was significantly correlated with daily mean mass concentrations of atmospheric PM averaged over 8 days before sample collection.
Conclusions
We demonstrated that apical stimulation with DEPs and LPS can significantly alter the basal secretome in PNHE, and this alteration can be reflected by surrounding inflammation with effusion of fluids in vivo such as MEEs in OM patients.
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