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产毒素多杀性巴氏杆菌诱导的猪萎缩性鼻炎的发病机制。

The pathogenesis of atrophic rhinitis in pigs induced by toxigenic Pasteurella multocida.

作者信息

Pedersen K B, Elling F

出版信息

J Comp Pathol. 1984 Apr;94(2):203-14. doi: 10.1016/0021-9975(84)90041-0.

Abstract

The pathogenesis of atrophic rhinitis was studied in an experiment in which piglets were infected with a toxigenic type D Pasteurella multocida strain in the right half of the nasal cavity. Two days before inoculation the nasal mucosa on the right side had been subjected to mild irritation by intranasal instillation of a weak solution of acetic acid. The untreated (left) half of the nasal cavity served as an intrinsic control. Macroscopically, changes in the turbinates were already appreciable at 3 days p.i., and pronounced turbinate atrophy was noted at 7 days p.i. At 14 days p.i. deviation of the snout and almost complete turbinate atrophy was observed. The turbinates in the untreated half of the nasal cavity developed normally. Histologically, the changes were initially characterized by bone resorption mediated by an increased number of osteoclasts. Later osteoclasts were sparse, and there was an apparent disruption of osteoid synthesis. Ultrastructurally, the osteoblasts showed nuclear indentations and dilatation of the endoplasmic reticulum. Since no inflammatory reaction was observed, the hypothesis is advanced that atrophic rhinitis in pigs is caused by a P. multocida-produced factor which will stimulate bone resorption and suppress osteoid synthesis.

摘要

在一项实验中对萎缩性鼻炎的发病机制进行了研究,该实验中,仔猪右侧鼻腔感染了产毒素的D型多杀性巴氏杆菌菌株。接种前两天,右侧鼻黏膜通过鼻内滴注稀醋酸溶液受到轻度刺激。未处理的(左侧)鼻腔作为自身对照。宏观上,感染后3天鼻甲变化已明显可见,感染后7天可见明显的鼻甲萎缩。感染后14天观察到口鼻歪斜和几乎完全的鼻甲萎缩。鼻腔未处理一侧的鼻甲正常发育。组织学上,变化最初表现为破骨细胞数量增加介导的骨吸收。后来破骨细胞稀少,类骨质合成明显中断。超微结构上,成骨细胞显示核凹陷和内质网扩张。由于未观察到炎症反应,因此提出假说,猪萎缩性鼻炎是由多杀性巴氏杆菌产生的一种因子引起的,该因子会刺激骨吸收并抑制类骨质合成。

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