title: A prophylactic effect of an oligodeoxynucleotide containing a cytidine-guanosine motif against Japanese cedar pollen-induced T-helper type 2 allergic response.
abstract: BACKGROUND
  Over 10% of entire population in Japan suffer from allergic diseases induced by Japanese cedar pollen (JCP) every spring. In terms of preventive medicine, it has become a matter of urgency to establish successful prophylactic and therapeutic strategies for controlling the disorders. The effect of an oligodeoxynucleotide containing a cytidine-guanosine motif (CpG ODN) on the regulation of immune responses induced by JCP was investigated in this study.
  
  
  METHODS
  BALB/c mice were inoculated with CpG ODN intraperitoneally before intranasal sensitization to JCP. Cellular infiltration in the lung of BALB/c mice after treatment with CpG ODN or JCP was performed by hematoxylin and eosin (H&E) staining. Antibody titers and cytokines levels were determined by ELISA.
  
  
  RESULTS
  Intranasal inoculation of BALB/c mice with JCP induced a T-helper type 2 (Th2-type) dominant immune response, as characterized by the production of interleukin (IL)-4 and IL-5 in the lung and of JCP-specific IgE antibody in serum. Prior intraperitoneal administration of CpG ODN to mice suppressed the subsequent JCP-induced antibody production and infiltration of inflammatory cells in the lung. The inhibitory mechanism of CpG ODN seemed to be attributable to a CpG ODN-induced Th1-type dominant environment, which down-regulated Th2-type response subsequently induced by JCP allergen sensitization. Furthermore, administration with CpG ODN decreased the production of JCP-induced IL-17, which has been found to play a pivotal role in several inflammatory diseases including allergic asthma. The decreased production of IL-17, together with reduced secretion of IL-4 and IL-5, may contribute to diminish the inflammation in the lung of JCP-sensitized mice.
  
  
  CONCLUSIONS
  This work provides evidence that the CpG ODN has a prophylactic effect on the JCP-induced Th2-type allergic responses by establishing or restoring a Th1-type shift of immune environments.
authors.affiliation: Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, PR China. bxliu@mail.cmu.edu.cn
authors.forename: Beixing
authors.initials: B
authors.lastname: Liu
authors.forename: Leiying
authors.initials: L
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Fengping
authors.initials: F
authors.lastname: Shan
authors.forename: Enhua
authors.initials: E
authors.lastname: Wang
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Kimura
mesh_terms: D000485:Allergens / Q000009:adverse effects*; D000818:Animals; D032485:Cryptomeria; D003562:Cytidine / Q000627:therapeutic use*; D015226:Dinucleoside Phosphates / Q000627:therapeutic use*; D006151:Guanosine / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009838:Oligodeoxyribonucleotides / Q000627:therapeutic use*; D011058:Pollen; D012130:Respiratory Hypersensitivity / Q000276:immunology* / Q000517:prevention & control*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D000485:Allergens; D015226:Dinucleoside Phosphates; D009838:Oligodeoxyribonucleotides; D006151:Guanosine; D003562:Cytidine