title: Imbalance of Th1 and Th2 cells in cardiac injury induced by ambient fine particles.
abstract: The study was to explore the potential immunoregulatory mechanisms linking fine particles and cardiac injury. Wistar kyoto (WKY) rats were exposed by intratracheal instillation to fine particles with the doses of 0.0, 1.6, 8.0 and 40.0mg/kg b.w., respectively. The exposure was conducted once a day, for three consecutive days. Twenty-four hours after the last exposure, the rats were sacrificed. Th1- and Th2-related transcription factors and cytokines were assessed in left ventricle of rats. The mRNA expressions of Th1- and Th2-related transcription factors signal transducer and activator of transcriptionl 1 (STAT1), signal transducer and activator of transcriptional 6 (STAT6), GATA-3 and T-bet were assessed in left ventricle of rats using real-time PCR. Meanwhile, the levels of Th1- and Th2-related cytokines IL-4, IL-13 and interferon gamma (IFN-γ) were determined by ELISA kits in cardiac homogenate supernatant of rats. Furthermore, the protein expression of IL-4 and IFN-γ were detected in myocardium by Western blot. The results of cardiac histology demonstrated exacerbated cardiac lesions and histological characterization of inflammation and degeneration in rats after exposure to fine particles. Moreover, fine particles induced significant increase of IL-4 and IL-13 and decrease of IFN-γ in myocardium of rats. The mRNA expression of STAT1, STAT6 and GATA-3 were up-regulated in left ventricle of rats in a dose-dependent manner, whereas T-bet was significantly down-regulated. The variations of these cytokines demonstrated the imbalance of Th1 and Th2 cytokines existed in cardiac injuries induced by fine particle. The imbalance of Th1/Th2 cytokines might be one of the mechanisms of immunotoxicity of cardiovascular system induced by ambient fine particles.
authors: Department of Environment Health, School of Public Health, Fudan University, the Key Laboratory of Public Health Safety, Ministry of Education, Shanghai 200032, China.
authors: Jinzhuo
authors: J
authors: Zhao
authors: Yuquan
authors: Y
authors: Xie
authors: Chunyan
authors: C
authors: Qian
authors: Li
authors: L
authors: Li
authors: Rongfang
authors: R
authors: Jiang
authors: Haidong
authors: H
authors: Kan
authors: Ruizhen
authors: R
authors: Chen
authors: Weimin
authors: W
authors: Song
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D050990:GATA3 Transcription Factor / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D052638:Particulate Matter / Q000633:toxicity*; D012333:RNA, Messenger / Q000737:chemistry / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D011921:Rats, Inbred WKY; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050794:STAT1 Transcription Factor / Q000096:biosynthesis / Q000235:genetics; D050800:STAT6 Transcription Factor / Q000235:genetics / Q000276:immunology; D013047:Specific Pathogen-Free Organisms; D018709:Statistics, Nonparametric; D020825:T-Box Domain Proteins / Q000096:biosynthesis / Q000235:genetics; D018417:Th1 Cells / Q000187:drug effects / Q000473:pathology*; D018418:Th2 Cells / Q000187:drug effects / Q000473:pathology*; D000098815:T-bet Transcription Factor
chemical_list: D016207:Cytokines; D050990:GATA3 Transcription Factor; D052638:Particulate Matter; D012333:RNA, Messenger; D050794:STAT1 Transcription Factor; D050800:STAT6 Transcription Factor; C494081:Stat1 protein, rat; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor