Winchurch R A, Hilberg C, Birmingham W, Munster A M
Immunology. 1982 Jan;45(1):147-53.
The effects of bacterial lipopolysaccharides (LPS) on the suppressor activity of mouse spleen cells were examined. Pretreatment with LPS was shown to induce suppressor activity in vivo and in vitro. Concurrent treatment of spleen cells with LPS and imidazole, an agent which increases the activity of cyclic nucleotide phosphodiesterases and hastens the degradation of cyclic AMP, reversed the suppressor-inducing effects of LPS. In vitro treatment of spleen cells with aminophylline, an agent which inhibits phosphodiesterase activity, had no effect on suppressor activity. The reversal of LPS-induced suppressor activity by imidazole was time-dependent and addition of this agent 20 hr after LPS treatment did not reverse suppression. These data are consistent with the hypothesis that LPS-induced suppressor activity may be mediated via cyclic AMP-dependent pathways.
研究了细菌脂多糖（LPS）对小鼠脾细胞抑制活性的影响。结果显示，LPS预处理可在体内和体外诱导抑制活性。用LPS和咪唑同时处理脾细胞，咪唑是一种可增加环核苷酸磷酸二酯酶活性并加速环磷酸腺苷降解的试剂，可逆转LPS的抑制诱导作用。用氨茶碱（一种抑制磷酸二酯酶活性的试剂）对脾细胞进行体外处理，对抑制活性没有影响。咪唑对LPS诱导的抑制活性的逆转具有时间依赖性，在LPS处理20小时后添加该试剂并不能逆转抑制作用。这些数据与以下假设一致，即LPS诱导的抑制活性可能通过环磷酸腺苷依赖性途径介导。
