title: [Dysfunction of releasing adrenaline in asthmatic adrenaline medullary chromaffin cells due to functional redundancy primed by nerve growth factor].
abstract: OBJECTIVE
  To investigate the possible causes of the dysfunction of adrenaline release in asthma rats and to identify the role of nerve growth factor (NGF) in this process.
  
  
  METHODS
  Thirty-two SD rats were randomly divided into four groups: control group (n = 8), asthma group (n = 8), NGF group (n = 8) and anti-NGF group (n = 8). The rats of asthma group, NGF group and anti-NGF group were sensitized and challenged with ovalbumin (OVA), and then NGF group and anti-NGF group were treated with NGF and anti-NGF, respectively. Adrenal glands were obtained for electron microscopic examination. The expression of phenylethanol-amine N-methyltransferase (PNMT) was analyzed by immunohistochemistry combined with the micro-image analysis. The concentrations of adrenaline and noradrenaline in serum were measured by enzyme-linked-immunosorbent assay (ELISA).
  
  
  RESULTS
  The data from the electron microscopy showed: (1) Compared with the control group, the number of mitochondria increased, while the concentration of the chromaffin granula decreased in asthma, NGF and anti-NGF groups. (2) There were some drumstick-like and villiform processes in the adrenaline medullary chromaffin cells (AMCC) membrane of the NGF group. The results of immunohistochemistry showed that the average gray value of PNMT of the NGF group was 218 +/- 38, which was significantly higher than those in the control group (182 +/- 25), asthma group (198 +/- 33) and anti-NGF group (195 +/- 41, t = 23.42, 19.76, 17.93, all P < 0.05). Serum levels of adrenaline in the NGF group were (2.9 +/- 0.5) ng/ml. They were significantly lower than those in the control group (7.1 +/- 0.4) ng/ml, asthma group (5.9 +/- 1.7) ng/ml and anti-NGF group (5.7 +/- 0.6) ng/ml (t = 7.64, 5.41, 4.96, all P < 0.01). Serum levels of adrenaline in the asthma group were significantly lower than those in the control group (t = 5.64, P < 0.01). However, no difference was found between the asthma group and the anti-NGF group (t = 0.87, P > 0.05).
  
  
  CONCLUSIONS
  NGF can prime the functional redundancy of the adrenaline medullary chromaffin cells, which leads to the dysfunction of adrenaline release and hence the pathogenesis of asthma.
authors.affiliation: Department of Respiratory Disease, Xiangya Hospital, Central South University, Changsha 410008, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Cheng-ping
authors.initials: CP
authors.lastname: Hu
authors.forename: Jun-tao
authors.initials: JT
authors.lastname: Feng
mesh_terms: D000313:Adrenal Medulla / Q000166:cytology / Q000378:metabolism; D000818:Animals; D001249:Asthma / Q000378:metabolism*; D019439:Chromaffin Cells / Q000378:metabolism*; D004837:Epinephrine / Q000097:blood*; D008297:Male; D020932:Nerve Growth Factor / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D020932:Nerve Growth Factor; D009638:Norepinephrine; D004837:Epinephrine