Barnett J B, Soderberg L S, Menna J H
Toxicol Lett. 1985 May;25(2):173-83. doi: 10.1016/0378-4274(85)90079-7.
Previous studies in our laboratory have indicated that in utero chlordane exposure caused a significant enhancement in the survival of the offspring to influenza virus infection. Further studies, reported here, show that the non-specific delayed type hypersensitivity (DTH) response to oxazolone at 100 days of age, but not at 30 days of age, was significantly depressed. In contrast, the Con A-induced blastogenic response of spleen cells from chlordane-treated offspring was not depressed and was, in fact, significantly enhanced. However, neither the response to PHA nor to LPS mitogens was significantly altered. In utero exposure to chlordane significantly depressed the mixed lymphocyte reactivity (MLR) of spleen cells from male offspring, whereas females showed no significant alteration of MLR. The significant depression of the DTH and MLR responses supports our previous reports of enhanced survival of influenza virus infection following in utero exposure to chlordane, since active DTH contributes to the pathology of influenza virus infection in mice. The normal or enhanced T-cell mitogen response suggested that the chlordane-induced depression of DTH and MLR was not due to overt toxicity to T-cells.
我们实验室之前的研究表明，子宫内接触氯丹会显著提高后代对流感病毒感染的存活率。本文报道的进一步研究表明，100日龄时对恶唑酮的非特异性迟发型超敏反应（DTH）受到显著抑制，但30日龄时未受抑制。相比之下，氯丹处理过的后代脾脏细胞对刀豆蛋白A诱导的增殖反应未受抑制，实际上还显著增强。然而，对PHA和LPS丝裂原的反应均未发生显著改变。子宫内接触氯丹显著抑制了雄性后代脾脏细胞的混合淋巴细胞反应性（MLR），而雌性后代的MLR未发生显著改变。DTH和MLR反应的显著抑制支持了我们之前关于子宫内接触氯丹后流感病毒感染存活率提高的报道，因为活跃的DTH会导致小鼠流感病毒感染的病理变化。正常或增强的T细胞丝裂原反应表明，氯丹诱导的DTH和MLR抑制并非由于对T细胞的明显毒性。
