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Title: [Activation of transcription factors and induction of cytokines from macrophages in chronic obstructive pulmonary disease]. Author: He B, Zhao M, Qi G. Journal: Zhonghua Yi Xue Za Zhi; 2001 Nov 25; 81(22):1360-4. PubMed ID: 11930628. Abstract: 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. CONCLUSION: 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.[Abstract] [Full Text] [Related] [New Search]