title: [The roles of interleukin-5 and eotaxin in signal transmission between lung and bone marrow of rat asthmatic models].
abstract: OBJECTIVE
  To explore the roles of interleukin-5 (IL-5) and eotaxin in signal transmission between lung and bone marrow in rat asthmatic models and to investigate the effects of different interventions on the signal transmission.
  
  
  METHODS
  Forty Wistar rats were randomly assigned to a control group and an asthma group (20 in each group). The asthmatic model were established by ovalbumin (OVA) sensitizing and challenging. The animals were sacrificed 30 min, 6 h, 12 h, 24 h, and 48 h after challenging, respectively. Slides were prepared from peripheral blood, bone marrow, and lung tissue respectively, and stained with HE. Then the total number and percentage of eosinophils (EOS) were counted. The concentrations of IL-5 and eotaxin in the lung homogenate at the different time points were determined by Enzyme-linked immunosorbent assay (ELISA). The bone marrow cells of the control rats and sensitized rats were incubated with lung homogenate of the different time points, and treated with dexamethasone (DXM), Galectin-3, anti-IL-5 polyclonal antibody, and montelukast, respectively. The bone marrow cell slides were stained with anti-IL-5 polyclonal antibody, anti-IL-5Ralpha polyclonal antibody, anti-eotaxin polyclonal antibody, anti-CD(34) polyclonal antibody, and anti-CCR(3) polyclonal antibody, respectively. The EOS and immunoactive cells were counted and represented as percentages of the total cells.
  
  
  RESULTS
  The percentages of EOS in peripheral blood, bone marrow, and lung tissue from the asthma group were 0.0200 +/- 0.0020, 0.023 +/- 0.003, 0.0250 +/- 0.0090, and those from the control group were 0.0100 +/- 0.0030, 0.009 +/- 0.003, 0.0090 +/- 0.0020 respectively. The differences were significant between the two groups (t = 2.547, 2.718, 2.718, all P < 0.05). The peak levels of IL-5 and eotaxin were (89.3 +/- 2.4) pg/ml at 6 h and (4.9 +/- 0.5) pg/ml at 12 h after allergy challenge, respectively, then the levels returned to the baseline value after 48 h (1.45 +/- 0.23) pg/ml. Except at 30 min, all other lung homogenate samples induced the increase of percentages of IL-5(+), IL-5Ralpha(+), eotaxin(+), CD(34)(+) and CCR(3)(+) immunoactive cells. After treatment with Galectin-3, the percentages of IL-5(+), IL-5Ralpha(+), eotaxin(+), CD(34)(+) and CCR(3)(+) immunoactive cells decreased to 0.021 +/- 0.005, 0.074 +/- 0.007, 0.138 +/- 0.014, 0.067 +/- 0.010, 0.040 +/- 0.005, 0.087 +/- 0.012.
  
  
  CONCLUSIONS
  Galectin-3, a selective inhibitor of IL-5 mRNA transcription, potentially suppresses eosinophilic inflammation and might be a promising specific anti-asthma agent.
authors.affiliation: Department of Respiratory Medicine, West China Hospital, Chengdu 610041, China.
authors.forename: Chun-tao
authors.initials: CT
authors.lastname: Liu
authors.forename: Ke
authors.initials: K
authors.lastname: Wang
authors.forename: Lian
authors.initials: L
authors.lastname: Li
authors.forename: Ya-min
authors.initials: YM
authors.lastname: Pang
mesh_terms: D000818:Animals; D001249:Asthma / Q000378:metabolism*; D001853:Bone Marrow / Q000378:metabolism*; D001854:Bone Marrow Cells / Q000378:metabolism; D054413:Chemokine CCL11 / Q000378:metabolism*; D004804:Eosinophils / Q000378:metabolism; D037502:Galectin 3 / Q000494:pharmacology; D015848:Interleukin-5 / Q000378:metabolism*; D008168:Lung / Q000378:metabolism*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction
chemical_list: D054413:Chemokine CCL11; D037502:Galectin 3; D015848:Interleukin-5