[Activation of transcription factors and induction of cytokines from macrophages in chronic obstructive pulmonary disease].
OBJECTIVE
To investigate the activation of transcription factors and induction of cytokines from alveolar macrophages in chronic obstructive pulmonary disease (COPD).


METHODS
Alveolar macrophages were collected by fibrobronchoscopy from 8 patients with chronic bronchitis, 8 patients with COPD, and 8 healthy volunteers. All patients were at stable stage. The macrophages thus collected were cultured and stimulated with lipopolysaccharide (LPS, 10 micrograms/ml). The IL-8, IL-1 beta, TNF alpha and IL-6 thus produced were measured by ELISA in the supernatant. Nuclear factor-kappa B (NF kappa B), activator protein-1 (AP-1), AP-2 and AP-3 were detected by electrophoretic mobility shift assay.


RESULTS
The concentration of IL-8 released from macrophages of patients with COPD at stable stage before LPS stimulation was about 3 times higher than that in the healthy control (F = 4.34, P < 0.05). The concentration of IL-8 released from macrophages in patients with COPD was increased further after LPS stimulation in comparison to that in healthy controls(F = 3.56, P < 0.05). The concentration of IL-1 beta and that of TNF alpha released from macrophages of COPD patients were further increased after LPS stimulation (P < 0.05) in the COPD patients, but there was no difference in the concentration of IL-1 beta and between the control and COPD patients before LPS stimulation. The constitutive activity of AP-1 and the activity of NF kappa B induced by LPS were higher in the patients with COPD than in the controls.


CONCLUSIONS
The alverlar macrophages of patients with COPD at stable stage may release higher concentration of IL-8 and IL-1 beta. LPS stimulation increases the release of IL-1 beta and TNF alpha of alveolar macrophages. Enhancement of activity of NF kappa B and AP-1 may positively regulate the production of IL-8 and IL-1 beta in the airflow obstruction.
He
B
B
Pulmonary Division, Department of Internal Medicine, Peking University, Third Hospital, Beijing 100083, China.
Zhao
M
M
Qi
G
G
D000328:Adult; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D016676:Macrophages, Alveolar / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism*; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D008070:Lipopolysaccharides; D016328:NF-kappa B; D018808:Transcription Factor AP-1; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha