title: Diesel exhaust particles selectively induce both proinflammatory cytokines and mucin production in cornea and conjunctiva human cell lines.
abstract: OBJECTIVE
  To evaluate the effect of diesel exhaust particles (DEP) on the viability, proliferation, apoptosis, secretion of cytokines (IL-6, IL-8, and TNF-α), and mucin gene transcription (MUC1, MUC5AC, and MUC16) in human epithelial cells of the cornea (HCLE) and conjunctiva (IOBA-NHC).
  
  
  METHODS
  HCLE and IOBA-NHC cells were incubated with DEP (10-500 μg/mL) for 24 hours. Cell proliferation was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptotic cells were measured by an annexin V-FITC and propidium iodide kit for flow cytometry. Proinflammatory cytokines were determined by an ELISA kit. Mucin gene transcription was quantified by real-time PCR.
  
  
  RESULTS
  DEP significantly decreased the viability, proliferation, and secretion of IL-8, but increased the secretion of IL-6 on both HCLE and IOBA-NHC cell lines in a dose-dependent manner. Neither cornea nor conjunctiva cells incubated with DEP released TNF-α. DEP induced a significant increase in the percentage of apoptotic cells in IOBA-NHC, whereas no changes were observed in HCLE. Finally, DEP significantly decreased the transcription levels of MUC1 and MUC16 in HCLE, but increased the transcription levels of MUC1, MUC5AC, and MUC16 in IOBA-NHC.
  
  
  CONCLUSIONS
  These findings suggest that human corneal and conjunctival epithelial cells incubated with DEP showed cytotoxicity and an inflammatory response mediated by IL-6, not by TNF-α or IL-8. Also, the decrease in mucin expression in the cornea cells might leave exposed areas in the cornea for contact with DEP. Finally, the increase in mucin expression in the conjunctiva cells might be involved at least in the clearance of DEP to protect the ocular epithelium.
authors.affiliation: Laboratorio de Investigaciones Oculares, Departamento de Patologí, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina. julia_tau@hotmail.com
authors.forename: Julia
authors.initials: J
authors.lastname: Tau
authors.forename: Priscila
authors.initials: P
authors.lastname: Novaes
authors.forename: Monique
authors.initials: M
authors.lastname: Matsuda
authors.forename: Deborah R
authors.initials: DR
authors.lastname: Tasat
authors.forename: Paulo H
authors.initials: PH
authors.lastname: Saldiva
authors.forename: Alejandro
authors.initials: A
authors.lastname: Berra
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D017209:Apoptosis / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003228:Conjunctiva / Q000166:cytology / Q000378:metabolism*; D003315:Cornea / Q000166:cytology / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D009077:Mucins / Q000235:genetics / Q000378:metabolism*; D052638:Particulate Matter / Q000633:toxicity*; D060888:Real-Time Polymerase Chain Reaction; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D016207:Cytokines; D009077:Mucins; D052638:Particulate Matter; D001335:Vehicle Emissions
keywords: conjunctiva; corneal epithelium; diesel