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Two different combination protocols were used: IL\u20101 and Ace were administered simultaneously; and IL\u20101 was injected 60 min after Ace administration (sequential exposure). Ace, in a dose\u2010 and time\u2010dependent manner, inhibited blood and brain acetylcholinesterase (AChE) activities, increased blood corticosterone concentrations, suppressed blood CD4, CD8, B cell and monocyte contents and increased blood neutrophil counts. The Ace\u2010induced changes lasted for up to 24 h after Ace exposure. Interleukin 1 increased blood corticosterone concentrations without affecting blood or brain AChE activities. The IL\u20101\u2010induced corticosterone concentration returned to the basal level within 3\u201310 h after IL\u20101 exposure. The CD4, CD8, B cell and monocyte counts increased significantly at 10 min after IL\u20101 exposure. The cell counts decreased gradually thereafter and returned to the basal level within 30 min after IL\u20101 exposure. Simultaneous exposure of rats to Ace and IL\u20101 partially suppressed the IL\u20101\u2010induced increase in the immune cell counts and decreased the immune cell numbers below the basal values. Sequential injection of Ace and IL\u20101 blocked the IL\u20101\u2010induced increase in the immune cell numbers. Thus, Ace exposure would impair the normal distribution of immune cells and deregulate the IL\u20101 response in rats. 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\u2010phase response, which would augment the toxic effects of IL\u20101 and other cytokines, and Ace exposure occurring prior to the injury would suppress or abolish the initial stimulatory effects of IL\u20101, which would decrease an organism's ability to combat infection or injury. 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