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仙台病毒肺炎期间蛋白质缺乏小鼠的组织病理学改变:炎症反应和恢复延迟的证据

Altered histopathology in protein-deprived mice during Sendai virus pneumonia: evidence for delayed inflammatory response and recovery.

作者信息

Peña-Cruz V, Bronson R T, Reiss C S, McIntosh K

机构信息

Division of Infectious Diseases, Children's Hospital, Boston, MA 02115.

出版信息

J Infect Dis. 1992 May;165(5):846-51. doi: 10.1093/infdis/165.5.846.

Abstract

The morphology of the lungs and airway during the course of respiratory infection caused by Sendai virus was examined in normal (20% protein diet) and malnourished (2% protein diet) BALB/c mice. Mortality in normal Sendai-infected mice was 0 compared with 71% in the infected malnourished group. Virus was isolated until day 6 in normally fed mice and until day 9 in the malnourished group. Pulmonary inflammation was largely mononuclear and began in the normally nourished animals on day 3, peaked at day 6, and reverted almost to normal by 30 days. In the malnourished group, inflammation was delayed by about 1 day and fell further behind during the first week. It peaked 10-13 days after infection and was still present with little resolution by day 30. These findings may have relevance to the high mortality of acute respiratory diseases in children of the developing world.

摘要

在正常(20%蛋白质饮食)和营养不良(2%蛋白质饮食)的BALB/c小鼠中,研究了仙台病毒引起的呼吸道感染过程中肺和气道的形态。正常感染仙台病毒的小鼠死亡率为0,而感染的营养不良组为71%。在正常喂食的小鼠中,病毒一直可分离到第6天,而在营养不良组中可分离到第9天。肺部炎症主要为单核细胞炎症,在营养正常的动物中于第3天开始,第6天达到峰值,到30天时几乎恢复正常。在营养不良组中,炎症延迟约1天出现,在第一周进一步滞后。它在感染后10 - 13天达到峰值,到30天时仍存在且几乎没有消退。这些发现可能与发展中国家儿童急性呼吸道疾病的高死亡率有关。

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Sendai viral pneumonia in aged BALB/c mice.老年BALB/c小鼠的仙台病毒性肺炎
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