title: [The expressions of nerve growth factor and its tyrosine kinase A receptor on alveolar macrophages in a rat model of chronic obstructive pulmonary disease].
abstract: OBJECTIVE
  To observe the expressions of nerve growth factor (NGF) and its tyrosine kinase A (TrkA) receptor on alveolar macrophage in a rat model of chronic obstructive pulmonary disease (COPD).
  
  
  METHODS
  Forty healthy male SD rats were randomly divided into a control group and a COPD group. The COPD model was established by exposing the rats to cigarette smoke for 6 months, and lung function changes were measured. Lung histopathological changes were detected by HE staining. The expression of NGF protein in the supernatant of alveolar macrophage (AM) culture medium was detected by ELISA. Confocal microscopy was used to identify the separation and purification of AM from bronchoalveolar lavage fluid, and to detect semi-quantitatively the expression of TrkA receptor on AM. NGF and its TrkA receptor at the mRNA level were evaluated by real-time PCR. The differences among groups were calculated by one way ANOVA, and comparison between groups was made by t test.
  
  
  RESULTS
  Significant decrease of pulmonary compliance [(0.15 ± 0.03) ml/cm H(2)O (1 cm H2O = 0.098 kPa)] and minute ventilation [(0.045 ± 0.004) L], and significant increase of airway resistance [(0.038 ± 0.004) cm H2O×L(-1)×s(-1)] were found in the COPD group compared with the control group [(0.42 ± 0.05) ml/cm H2O and (0.102 ± 0.010) L and (0.016 ± 0.002) cm H2O×L(-1)×s(-1), t = 9.46 - 12.99, respectively, all P < 0.01]. Alveolar wall thinning, alveolar septa breakdown, alveolar enlargement and emphysema were significant in the COPD rats. The expression of NGF protein in the supernatant of AM culture medium was enhanced in the COPD group [(3.79 ± 1.52) ng/L] compared with the controls [(0.94 ± 0.27) ng/L, t = 4.13, P < 0.05]. Mean fluorescence intensity of TrkA protein on AM in the COPD group (19.5 ± 1.5) was higher than that in the control group (11.2 ± 1.9, t = 7.95, P < 0.05). The expressions of NGF and TrkA at mRNA level in the COPD group (24.8 ± 6.0 and 9.0 ± 3.3) were increased compared with the control group (1.0 ± 0.2 and 1.0 ± 0.4, t = 8.48 and 5.16, all P < 0.05).
  
  
  CONCLUSIONS
  The expressions of NGF and its TrkA receptor on AM in COPD group were increased, indicating that NGF and its TrkA receptor might be involved in the pathogenesis of COPD mediated by AM.
authors.affiliation: Department of Respiratory and Critical Care Medicine, Nanjing University Clinical School of Medicine, Nanjing General Hospital of Nanjing Military Command, Nanjing 210002, China.
authors.forename: Miao-miao
authors.initials: MM
authors.lastname: Li
authors.forename: Xiao-feng
authors.initials: XF
authors.lastname: Xin
authors.forename: Hong-tao
authors.initials: HT
authors.lastname: Shao
authors.forename: Yi
authors.initials: Y
authors.lastname: Shi
authors.forename: Xin
authors.initials: X
authors.lastname: Su
authors.forename: Wen-kui
authors.initials: WK
authors.lastname: Sun
authors.forename: He
authors.initials: H
authors.lastname: Sun
authors.forename: Li-ping
authors.initials: LP
authors.lastname: Fang
mesh_terms: D000818:Animals; D016676:Macrophages, Alveolar / Q000378:metabolism* / Q000473:pathology; D008297:Male; D020932:Nerve Growth Factor / Q000378:metabolism*; D011650:Pulmonary Alveoli / Q000166:cytology / Q000378:metabolism*; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020917:Receptor, trkA / Q000378:metabolism*
chemical_list: D020932:Nerve Growth Factor; D020917:Receptor, trkA