title: [Airway inflammation and macrophage inflammatory protein-1alpha, gelatinase B level in patients with COPD].
abstract: OBJECTIVE
  To investigate the levels of macrophage inflammatory protein-1alpha (MIP-1alpha) and gelatinase-B (MMP-9) in bronchial alveolar lavage fluids (BALF) and supernatants of the cultured alveolar macrophages (AM) in patients with chronic bronchitis (CB) and chronic obstructive pulmonary disease (COPD).
  
  
  METHODS
  Bronchial alveolar lavage (BAL) was performed bronchoscopically in CB group, COPD group, and control group. Total cells were counted using hemacytometer. Differential cell counts were made with Wright's stained cell smear. The levels of MIP-1alpha, MMP-9 in BALF and in supernatants of cultured AMs were measured by ELISA.
  
  
  RESULTS
  The numbers of AMs and neutrophils in BALF in patients with CB and COPD groups were significantly higher than those in control group (P < 0.05). The levels of MIP-1alpha and MMP-9 in BALF and the supernatants of cultured AMs in patients with CB and COPD groups were higher than those in control group (P < 0.05). The levels of MIP-1alpha and MMP-9 in BALF were positively correlated with those in the supernatants of cultured AMs (r = 0.253, P < 0.05; r = 0.529, P < 0.01). The number of AMs in BALF was positively correlated with the level of MIP-1alpha and MMP-9 in BALF (r = 0.558, P < 0.01; r = 0.405, P < 0.01). Both AMs counts and the levels of MIP-1alpha, MMP-9 in BALF were inversely correlated with FEV(1.0)%pred (r = -0.322, P < 0.05; r = -0.319, P < 0.05; r = -0.616, P < 0.01). The levels of MIP-1alpha and MMP-9 in supernatants of the culture AMs were increased significantly after LPS stimulation (P < 0.05).
  
  
  CONCLUSIONS
  AMs, which may be the most important cellular source of MIP-1alpha and MMP-9 in COPD, accelerate MIP-1alpha and MMP-9 accumulation in the lung, which exaggerates inflammation process in the airway.
authors.affiliation: Department of Respiratory Medicine, The Second Affiliated Hospital, Central South University, Changsha 410011, China.
authors.forename: S
authors.initials: S
authors.lastname: Cai
authors.forename: P
authors.initials: P
authors.lastname: Chen
authors.forename: Y
authors.initials: Y
authors.lastname: Zhu
mesh_terms: D000328:Adult; D029481:Bronchitis, Chronic / Q000378:metabolism* / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002452:Cell Count; D002478:Cells, Cultured; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D003470:Culture Media; D005260:Female; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000503:physiopathology; D019402:Macrophage Inflammatory Proteins / Q000378:metabolism*; D016676:Macrophages, Alveolar / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism*; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D054405:Chemokine CCL3; D054407:Chemokine CCL4; D003470:Culture Media; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins; D020780:Matrix Metalloproteinase 9