title: Effects of ozone exposure mediated by BEAS-2B cells on T cells activation: a possible link between environment and asthma.
abstract: OBJECTIVE
  To explore the possible link between ozone and asthma through analyzing Th1/Th2 differentiation of T cells following incubation with conditioned medium from the BEAS-2B cells exposed to ozone in vitro.
  
  
  METHODS
  Bronchial epithelial cell line, BEAS-2B, was cultured using an air-liquid interface culture system in a CO2 incubator and exposed to 0 or 0.16 or 0.25 mg/m3 of ozone for 8 h. The amounts of IL-1β, IL-6 and RANTES in the cell supernatant were detected. The cell culture supernatants were collected and used as conditioned medium in the next experiment. T cells from children recruited were incubated with conditioned medium for 12 h. Activation rate of CD69 and Th1/Th2/Th17 differentiation were analyzed.
  
  
  RESULTS
  BEAS-2B cells exposed to different ozone concentrations showed morphological changes. Cells exposed to 0.16 and 0.25 mg/m3 ozone produced higher amounts of IL-1β, IL-6 and RANTES than that in the control group. Children with allergic asthma had upregulated expression of genes related with asthma, including CCL2, CCR4, CXCL2, CYSLTR1, IL12RB2, IL13RA2, IL18R1, IL1B, IL8, IL8RB and TNFSF13.CD69 expression in T cells was significantly elevated irrespective of ozone exposure in children with allergic asthma. Following ozone exposure, in asthmatic children group, expression levels of cytokines of Th1 cells were collectively higher than those from Th2 cells. Ozone-exposed conditioned media could slightly increase all the Th1, Th2 and Th17 cytokines in T cells from allergic asthmatic children.
  
  
  CONCLUSIONS
  Our results suggested that Th1 cells activation might be predominant over Th2 activation upon ozone exposure in asthmatic children, which might help to clarify the mechanisms of asthma related to environmental factors like ozone.
authors.affiliation: Department of Preventive Medicine, School of Public Health, Sun Yat-Sen University, Guangzhou, P.R. China.
authors.forename: Dan
authors.initials: D
authors.lastname: Wu
authors.forename: Weipin
authors.initials: W
authors.lastname: Tan
authors.forename: Qiuli
authors.initials: Q
authors.lastname: Zhang
authors.forename: Xuchao
authors.initials: X
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Song
mesh_terms: D001249:Asthma / Q000139:chemically induced* / Q000276:immunology*; D001980:Bronchi / Q000276:immunology; D002460:Cell Line; D018946:Chemokine CCL5 / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D004781:Environmental Exposure / Q000009:adverse effects*; D004847:Epithelial Cells / Q000276:immunology; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology*; D010126:Ozone / Q000009:adverse effects* / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D018946:Chemokine CCL5; D053583:Interleukin-1beta; D015850:Interleukin-6; D010126:Ozone