Effect of diesel exhaust particles on human middle ear epithelial cells

Song, Jae Jun; Lee, Jong Dae; Lee, Byung Don; Chae, Sung Won; Park, Moo Kyun

doi:10.1016/j.ijporl.2011.12.003

Cited by 43 publications

(39 citation statements)

References 24 publications

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“…PM 2.5 induced MUC5AC mRNA in mouse trachea after 48 h of exposure, and MUC5AC mRNA and protein in human bronchial epithelial cells after 24 h of exposure [20]. Increased expression of MUC5AC by DEPs was also shown in human middle ear epithelial cells [10]. In the present study, we showed that DEPs induce MUC4 mRNA and protein expression in NCI-H292 cells and PNECs.…”

Section: Discussionsupporting

confidence: 64%

“…The relationship between DEPs and mucus secretion is another focus. In a study on human middle ear epithelial cells, exposure to DEPs increased the expression of MUC5AC, a secreted form of mucin [10]. Goblet cell hyperplasia of the nasal mucosa was also observed in a group of officers occupied with clearing diesel vehicles over 5 years [11].…”

Section: Introductionmentioning

confidence: 99%

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Diesel Exhaust Particles Enhance MUC4 Expression in NCI-H292 Cells and Nasal Epithelial Cells via the p38/CREB Pathway

Park

Kang

Kim

et al. 2016

Int Arch Allergy Immunol

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Background: Diesel exhaust particles (DEPs), the major contributors to air pollution, induce inflammatory responses in the nasal epithelium. Overproduction of airway mucins is an important pathogenic finding in inflammatory airway diseases. Objective: The aims of the present study were to determine the effect of DEPs on the expression of the mucin gene MUC4 and to investigate the underlying mechanism of DEP-induced MUC4 expression in NCI-H292 cells and primary nasal epithelial cells (PNECs). Methods: NCI-H292 cells were stimulated for 24 h with DEPs. Messenger RNA (mRNA) and protein expression of MUC4 was determined by real-time reverse transcription (RT) polymerase chain reaction (PCR) and Western blotting. NCI-H292 cells were exposed to 3 mitogen-activated protein kinase inhibitors (U0126, SB203580, and SP600125) and a CREB (cAMP response element-binding protein) inhibitor prior to stimulation with DEPs, and MUC4 expression was examined by RT-PCR and Western blotting. PNECs were pretreated with a p38 inhibitor and CREB inhibitor prior to stimulation with DEPs, and MUC4 expression was then determined by RT-PCR and/or Western blotting. Results: DEPs significantly increased the expression of MUC4 mRNA and protein. MUC4 mRNA and protein expression was inhibited by pretreatment with p38 and CREB inhibitors in NCI-H292 stimulated with DEPs. p38 and CREB inhibitors also blocked the expression of MUC4 mRNA and protein in DEP-stimulated PNECs. Conclusions: We demonstrated that DEPs stimulated the expression of MUC4 via the p38/CREB pathway in NCI-H292 cells and PNECs. The results of the present study pave the way for further studies on the role of MUC4 in DEP-induced hypersecretion in airway epithelium.

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Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Diesel Exhaust Particles Enhance MUC4 Expression in NCI-H292 Cells and Nasal Epithelial Cells via the p38/CREB Pathway

Park

Kang

Kim

et al. 2016

Int Arch Allergy Immunol

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“…Inflammatory cytokines, including COX-2, TNF-α, NF-κB, IL-1, IL-6, and IL-8, play a critical role in immune regulation, the initiation of mucosal changes, the inflammatory response in the middle ear, and stimulating mucin secretion [22,23] . Increased inflammatory cytokine and mucin gene expression have been demonstrated in cigarette smoke-and diesel-induced OM [9,10] . Inhalation of cadmium resulted in increased TNF-α, IL-6, and macrophage inflammatory protein (MIP-2) in rat lungs [24] .…”

Section: Discussionmentioning

confidence: 99%

“…The HMEECs were kindly provided by Dr. David J. Lim [12] and were grown, as previously described [10] . Briefly, we mixed Dulbecco's modified Eagle's medium (DMEM) and bronchial epithelial basal medium (BEBM) (1:1) with other supplements to make growth medium: bovine pituitary extract (52 µg/mL), hydrocortisone (0.5 µg/mL), human epidermal growth factor (hEGF; 0.5 ng/mL), epinephrine (0.5 mg/mL), transferrin (10 µg/mL), insulin (5 µg/mL), triiodothyronine (6.5 ng/mL), retinoic acid (0.1 ng/mL), gentamycin (50 µg/mL), and amphotericin B (50 ng/mL).…”

Section: Cell Culturementioning

confidence: 99%

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Effect of Cadmium on Human Middle Ear Epithelial Cells

Song

Yoon²,

Kim

et al. 2016

Int Adv Otol

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OBJECTIVE: Cadmium (Cd 2+) exposure can occur through passive smoking, ambient air pollution, and food. Even low exposure can affect hearing and cause lung disease. Here we investigated whether cadmium causes cytotoxicity, induces inflammation, or increases mucin gene expression in immortalized human middle ear epithelial cells (HMEECs). MATERIALS and METHODS:Cell viability was investigated using the MTT assay following Cd 2+ treatment. Increases in apoptosis and necrosis were determined, and the production of reactive oxygen species (ROS) was measured. We analyzed the expression of an inflammatory cytokine (COX-2) gene and a mucin gene (MUC5AC) using RT-PCR. RESULTS: Exposure to >20 µM Cd2+ caused a significant decrease in cell viability. Hoechst 33258 staining showed apoptotic morphology of heterogeneous intensity, condensation, and fragmentation after Cd2+ exposure. Cd 2+ was shown to increase cell death by apoptosis and necrosis by annexin V-FITC/PI double staining. Cd 2+ exposure increased ROS production and COX-2 and MUC5AC expressions. CONCLUSION:Our findings suggest that environmental cadmium exposure is related to the development of otitis media.

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