Barnett J B, Holcomb D, Menna J H, Soderberg L S
Toxicol Lett. 1985 Jun;25(3):229-38. doi: 10.1016/0378-4274(85)90202-4.
Previous studies in our laboratory have documented that in utero chlordane exposure caused a significant enhancement in the survival of the offspring to influenza A virus infection, and a depressed delayed type hypersensitivity (DTH) response to oxazolone. To correlate these 2 effects, we assayed influenza A virus-specific DTH response, and found that it was significantly decreased in chlordane-treated offspring. Virus-specific T-cell blastogenesis was also assayed in chlordane-treated animals. No significant differences due to the chlordane treatment were found in virus-specific T-cell blastogenesis, suggesting that the DTH depression did not result from a paucity of antigen-reactive T-cells. To determine whether enhanced survival was due, in part, to the effects of chlordane on virus replication, rather than on immunological alteration alone, the kinetics of influenza virus replication in the lungs of chlordane- and vehicle-treated animals were determined. In utero chlordane treatment caused no significant differences in in vivo virus replication. These data suggest that increased survival was due to a decrease in virus-specific DTH and its associated pathology.
我们实验室之前的研究表明，子宫内接触氯丹会导致后代对甲型流感病毒感染的存活率显著提高，同时对恶唑酮的迟发型超敏反应（DTH）受到抑制。为了关联这两种效应，我们检测了甲型流感病毒特异性DTH反应，发现氯丹处理的后代中该反应显著降低。我们还在氯丹处理的动物中检测了病毒特异性T细胞增殖。未发现氯丹处理对病毒特异性T细胞增殖有显著差异，这表明DTH抑制并非源于抗原反应性T细胞数量不足。为了确定存活率提高是否部分归因于氯丹对病毒复制的影响，而非仅对免疫改变的影响，我们测定了氯丹处理和载体处理动物肺部流感病毒复制的动力学。子宫内氯丹处理对体内病毒复制无显著差异。这些数据表明，存活率提高是由于病毒特异性DTH及其相关病理学的降低。
