Qiu H B, Chen D C, Pan J Q, Liu D W, Ma S
Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Zhongguo Yao Li Xue Bao. 1999 Mar;20(3):271-5.
To observe the effects of nitric oxide and interleukin-10 (IL-10) on inflammatory reaction in mouse alveolar macrophages (AM).
AM from mice were stimulated by lipopolysaccharides (LPS) 10 mg.L-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 (TNF alpha), IL-1 beta, IL-6, and IL-10 by AM were measured by ELISA.
After LPS-stimulation, TNF alpha, IL-1 beta, and IL-6 peaked at 6, 12, and 24 h, respectively by AM. SMT inhibited LPS-induced nitric oxide release and increased IL-1 beta and IL-6 secretions in AM, but the TNF alpha levels remained unchanged. SNAP had inhibitory effects on IL-1 beta and IL-6 secretions in a concentration-dependent manner, but exerted no effect on TNF alpha release. TNF alpha, IL-1 beta, and IL-6 secretions were inhibited by recombinant IL-10, but the cytokines release was upregulated by anti-IL-10 monoclonal antibody.
Both endogenous and exogenous nitric oxide and IL-10 had inhibitory effects on the LPS-induced TNF alpha, IL-1 beta, and IL-6 secretions in mouse AM.
观察一氧化氮和白细胞介素-10(IL-10)对小鼠肺泡巨噬细胞(AM)炎症反应的影响。
用10mg.L-1脂多糖(LPS)、一氧化氮合酶抑制剂硫酸S-甲基异硫脲(SMT)或一氧化氮供体S-亚硝基-N-乙酰-D,L-青霉胺(SNAP)刺激小鼠的AM。采用酶联免疫吸附测定法检测AM产生的肿瘤坏死因子α(TNFα)、IL-1β、IL-6和IL-10。
LPS刺激后,AM产生的TNFα、IL-1β和IL-6分别在6、12和24小时达到峰值。SMT抑制LPS诱导的一氧化氮释放,并增加AM中IL-1β和IL-6的分泌,但TNFα水平保持不变。SNAP以浓度依赖的方式抑制IL-1β和IL-6的分泌,但对TNFα释放无影响。重组IL-10抑制TNFα、IL-1β和IL-6的分泌,但抗IL-10单克隆抗体上调细胞因子的释放。
内源性和外源性一氧化氮及IL-10均对LPS诱导的小鼠AM中TNFα、IL-1β和IL-6的分泌具有抑制作用。