Immunotoxicity of acute @entity43963 exposure in control or IL-1-challenged XXXX : correlation between the immune cell composition and corticosteroid concentration in blood.

@entity43963 @entity11264 @entity2819 @entity4833 @entity35 @entity130
@entity2819 concentration and the immune cell composition were measured in @entity35 exposed by intraperitoneal (i.p.) injection to different doses (10-500 mg kg(-1)) of @entity43963 (Ace) and 250 micro g kg(-1) of interleukin 1 (IL-1), either alone or in combination. Two different combination protocols were used: IL-1 and Ace were administered simultaneously; and IL-1 was injected 60 min after Ace administration (sequential exposure). Ace, in a dose- and time-dependent manner, inhibited blood and brain acetylcholinesterase ( @entity4833 ) activities, increased blood @entity2819 concentrations, suppressed blood @entity11264 , CD8, B cell and monocyte contents and increased blood neutrophil counts. The Ace-induced changes lasted for up to 24 h after Ace exposure. Interleukin 1 increased blood @entity2819 concentrations without affecting blood or brain @entity4833 activities. The IL-1-induced @entity2819 concentration returned to the basal level within 3-10 h after IL-1 exposure. The @entity11264 , CD8, B cell and monocyte counts increased significantly at 10 min after IL-1 exposure. The cell counts decreased gradually thereafter and returned to the basal level within 30 min after IL-1 exposure. Simultaneous exposure of @entity35 to Ace and IL-1 partially suppressed the IL-1-induced increase in the immune cell counts and decreased the immune cell numbers below the basal values. Sequential injection of Ace and IL-1 blocked the IL-1-induced increase in the immune cell numbers. Thus, Ace exposure would impair the normal distribution of immune cells and deregulate the IL-1 response in @entity35 . This study therefore suggests that Ace would suppress the immune cell numbers in blood, thus decreasing an organism's immunity. Ace exposure occurring concurrent with injury would augment the acute-phase response, which would augment the toxic effects of IL-1 and other cytokines, and Ace exposure occurring @entity130 would suppress or abolish the initial stimulatory effects of IL-1, which would decrease an organism's ability to combat @entity130 .
