Effects of ozone exposure mediated by BEAS-2B cells on T cells activation: a possible link between environment and asthma.
نویسندگان
چکیده
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. METHOD 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.
منابع مشابه
Signalling pathway of isophorone diisocyanate-responsive interleukin-8 in airway smooth muscle cells.
This study is the first to analyse the soluble factors secreted by the bronchial epithelium after exposure to isophorone diisocyanate (IPDI) that are responsible for increasing migration and proliferation of primary normal human bronchial smooth muscle cells (BSMCs). We treated immortalised, nontumorigenic human bronchial epithelial cells (cell line BEAS-2B) and primary normal human bronchial e...
متن کاملSrc-Mediated EGF Receptor Activation Regulates Ozone-Induced Interleukin 8 Expression in Human Bronchial Epithelial Cells
BACKGROUND Human exposure to ozone (O3) results in pulmonary function decrements and airway inflammation. The mechanisms underlying these adverse effects remain unclear. Epidermal growth factor receptor (EGFR) plays an important role in the pathogenesis of lung inflammation. OBJECTIVE We examined the role of EGFR activation in O3-induced expression of the chemokine interleukin 8 (IL-8) in hum...
متن کاملActivation of nuclear factor-kappaB and not activator protein-1 in cellular response to nickel compounds.
The predominant exposure route for nickel compounds is by inhalation, and several studies have indicated the correlation between nickel exposure and respiratory cancers. The tumor-promoting effects of nickel compounds are thought to be associated with their transactivation of transcription factors. We have investigated the possible activation of activator protein-1 (AP-1) and nuclear factor KB ...
متن کاملAdhesion of human lung mast cells to bronchial epithelium: evidence for a novel carbohydrate-mediated mechanism.
Mast cells contribute to the pathophysiology of asthma through their immunomediator-secretory activity in response to both immunological and nonimmunological stimuli, and infiltrate the bronchial epithelium in this disease. We hypothesized that human lung mast cells (HLMC) localize to the bronchial epithelium via a specific cell-cell adhesion mechanism. We investigated the adhesion of HLMC to p...
متن کاملBronchial epithelium-derived IL-8 and RANTES increased bronchial smooth muscle cell migration and proliferation by Krüppel-like factor 5 in areca nut-mediated airway remodeling.
This study is first to analyze the inflammatory cytokines, produced by the bronchial epithelium after exposure to areca nut extract (ANE), which contribute to airway remodeling by increasing human bronchial smooth muscle cells (BSMC) migration and proliferation. We treated human bronchial epithelial cell lines BEAS-2B and HBE135-E6E7 (HBE) with ANE, saliva-reacted ANE (sANE), and the areca alka...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Asian Pacific journal of allergy and immunology
دوره 32 1 شماره
صفحات -
تاریخ انتشار 2014