title: T-helper type 1-T-helper type 2 shift and nasal remodeling after fine particulate matter exposure in a rat model of allergic rhinitis.
abstract: BACKGROUND
  Exposure to fine particulate matter (particulate matter ≤2.5 μm [PM2.5]) increases the risk of allergic rhinitis (AR), but the underlying mechanisms remains unclear. Thus, we investigated the roles of T-helper (Th)1-Th2 cytokines and nasal remodeling after ambient PM2.5 exposure in a rat model of AR.
  
  
  METHODS
  Female Sprague-Dawley rats were randomized into six groups: a negative control group, a group of healthy rats exposed to 3000 μg/m3 PM2.5, an ovalbumin (OVA) induced AR model, and three PM2.5-exacerbated AR groups exposed to three different concentrations (200, 1000, and 3000 μg/m3) of PM2.5 for 30 days via inhalation. Nasal symptoms, levels of Th1-Th2 cytokines, the degree of eosinophilia in nasal lavage fluid (NLF), and the messenger RNA (mRNA) expressions of transcription factors GATA-3 and T-bet in the nasal mucosa were measured in each individual rat. Hyperplasia of globet cells and collagen deposition were examined by histology.
  
  
  RESULTS
  PM2.5 significantly increased the number of sneezes and nasal rubs in rats with AR. PM2.5 also significantly decreased interferon gamma and increased interleukin (IL) 4 and IL-13 expressions as well as the number of eosinophils in NLF. The mRNA expression of GATA-3 in the nasal mucosa of rats with AR was upregulated by PM2.5, whereas T-bet was significantly downregulated. Statistically significant differences in OVA-specific serum immunoglobulin E, goblet cell hyperplasia, collagen deposition, and transforming growth factor beta 1 levels were observed between the PM2.5-exacerbated AR groups and the AR model group.
  
  
  CONCLUSIONS
  Analysis of our data indicated that an increase in the immune response with Th2 polarization and the development of nasal remodeling may be the immunotoxic mechanisms behind the exacerbation of AR after exposure to PM2.5.
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Guo
authors.forename: Wei-Yang
authors.initials: WY
authors.lastname: Dong
authors.forename: Jian
authors.initials: J
authors.lastname: Xu
authors.forename: Zhi-Cong
authors.initials: ZC
authors.lastname: Hong
authors.forename: Ren-Wu
authors.initials: RW
authors.lastname: Zhao
authors.forename: Cong-Rui
authors.initials: CR
authors.lastname: Deng
authors.forename: Guo-Shun
authors.initials: GS
authors.lastname: Zhuang
authors.forename: Ru-Xin
authors.initials: RX
authors.lastname: Zhang
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004781:Environmental Exposure / Q000009:adverse effects; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D050990:GATA3 Transcription Factor / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation; D006801:Humans; D006965:Hyperplasia; D007073:Immunoglobulin E / Q000097:blood; D009297:Nasal Mucosa / Q000473:pathology*; D010047:Ovalbumin / Q000276:immunology; D052638:Particulate Matter / Q000009:adverse effects / Q000276:immunology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D065631:Rhinitis, Allergic / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology*; D058408:Th1-Th2 Balance; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D000485:Allergens; D016207:Cytokines; D050990:GATA3 Transcription Factor; D052638:Particulate Matter; D007073:Immunoglobulin E; D010047:Ovalbumin