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3-甲基吲哚和牛呼吸道合胞病毒在犊牛中引起的肺部病变

Pulmonary lesions induced by 3-methylindole and bovine respiratory syncytial virus in calves.

作者信息

Castleman W L, Lacy S, Slauson D O, Atz J

机构信息

Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison 53706.

出版信息

Am J Vet Res. 1990 Nov;51(11):1806-14.

PMID:2173450
Abstract

Our objectives were to describe the ultrastructural morphogenesis of pulmonary lesions induced by 3-methylindole in 30- to 45-day-old Holstein calves and to determine whether toxic exposure to 3-methylindole exacerbates pulmonary lesions induced by bovine respiratory syncytial virus. Administration of 3-methylindole (0.25 g/kg) to calves resulted in interstitial edema and ultrastructural swelling of type-I alveolar epithelial cells and nonciliated bronchiolar epithelial cells as early as 4 to 6 hours after intraruminal administration. More severe alveolar edema containing protein was associated with swelling of capillary endothelial cells at 2 days after administration. Proliferation of type-II alveolar epithelial cells was first observed at 2 days after 3-methylindole administration, and marked hyperplasia of type-II epithelial cells and nonciliated bronchiolar epithelial cells was evident by 4 days after administration. Pulmonary cytochrome P-450 monooxygenase concentrations decreased significantly (P less than 0.001) by 12 hours after administration and did not increase significantly again by 8 days after administration. Calves were inoculated with bovine respiratory syncytial virus 3 days after administration of 3-methylindole, and pulmonary lesions were assessed 5 days after viral inoculation. Viral replication was demonstrated by fluorescence microscopy for viral antigen or by transmission electron microscopy in ciliated and nonciliated airway epithelial cells. Viral antigen was identified infrequently in alveolar macrophages and in type-II alveolar epithelial cells. 3-Methylindole exposure in calves did not result in more widespread distribution of viral antigen in alveolar tissue of respiratory syncytial virus-inoculated calves or in significant enhancement of viral pneumonia.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们的目标是描述3 - 甲基吲哚在30至45日龄荷斯坦犊牛中诱导的肺部病变的超微结构形态发生,并确定3 - 甲基吲哚的毒性暴露是否会加剧牛呼吸道合胞病毒诱导的肺部病变。给犊牛瘤胃内注射3 - 甲基吲哚(0.25 g/kg)后,最早在注射后4至6小时,I型肺泡上皮细胞和无纤毛细支气管上皮细胞出现间质水肿和超微结构肿胀。给药2天后,含有蛋白质的更严重肺泡水肿与毛细血管内皮细胞肿胀有关。II型肺泡上皮细胞的增殖在3 - 甲基吲哚给药后2天首次观察到,给药4天后II型上皮细胞和无纤毛细支气管上皮细胞明显增生。给药后12小时,肺细胞色素P - 450单加氧酶浓度显著降低(P小于0.001),给药后8天未再次显著升高。在3 - 甲基吲哚给药3天后给犊牛接种牛呼吸道合胞病毒,并在病毒接种后5天评估肺部病变。通过病毒抗原的荧光显微镜检查或在纤毛和无纤毛气道上皮细胞中的透射电子显微镜检查来证明病毒复制。在肺泡巨噬细胞和II型肺泡上皮细胞中很少发现病毒抗原。犊牛暴露于3 - 甲基吲哚并未导致接种呼吸道合胞病毒的犊牛肺泡组织中病毒抗原更广泛的分布,也未导致病毒性肺炎的显著加重。(摘要截断于250字)

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