Inhibitory effects of nitric oxide and interleukin-10 on production of tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 in mouse alveolar macrophages
Qiu, H.B.; Chen, D.C.; Pan, J.Q.; Liu, D.W.; Ma, S.
Zhongguo Yao Li Xue Bao 20(3): 271-275
1999
ISSN/ISBN: 0253-9756 PMID: 10452106 Document Number: 511152
AIM: To observe the effects of nitric oxide and interleukin-10 (IL-10) on inflammatory reaction in mouse alveolar macrophages (AM). METHODS: AM from mice were stimulated by lipopolysaccharides (LPS) 10 mgcntdotL-1 and nitric-oxide synthase inhibitor, S-methylisothiorea sulfate (SMT) or nitric-oxide donor, S-nitroso-N-acetyl-D,L-penicillamine (SNAP). The production of tumor necrosis factor alpha (TNFalpha), IL-1beta, IL-6, and IL-10 by AM were measured by ELISA. RESULTS: After LPS-stimulation, TNFalpha, IL-1beta, and IL-6 peaked at 6, 12, and 24 h, respectively by AM. SMT inhibited LPS-induced nitric oxide release and increased IL-1beta and IL-6 secretions in AM, but the TNFalpha levels remained unchanged. SNAP had inhibitory effects on IL-1beta and IL-6 secretions in a concentration-dependent manner, but exerted no effect on TNFalpha release. TNFalpha, IL-1beta, and IL-6 secretions were inhibited by recombinant IL-10, but the cytokines release was upregulated by anti-IL-10 monoclonal antibody. CONCLUSION: Bothendogenous and exogenous nitric oxide and IL-10 had inhibitory effects on the LPS-induced TNFalpha, IL-1beta, and IL-6 secretions in mouse AM.