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由胞内劳森菌引起的猪增生性肠炎的早期发病机制。

Early pathogenesis in porcine proliferative enteropathy caused by Lawsonia intracellularis.

作者信息

Boutrup T S, Boesen H T, Boye M, Agerholm J S, Jensen T K

机构信息

National Veterinary Institute, Technical University of Denmark, Copenhagen, Denmark.

出版信息

J Comp Pathol. 2010 Aug-Oct;143(2-3):101-9. doi: 10.1016/j.jcpa.2010.01.006. Epub 2010 Feb 18.

DOI:10.1016/j.jcpa.2010.01.006
PMID:20167332
Abstract

The intestinal bacterium Lawsonia intracellularis, the cause of proliferative enteropathy (PE) in pigs, is believed to infect mitotically active epithelial cells of the intestinal crypts and then multiply and spread in these cells as they divide. Further spread of infection is thought to occur by shedding of bacteria from infected crypts followed by infection of new crypts. The early stages of the pathogenesis of PE, from 0 to 48 hours post-infection (hpi), have not been studied in vivo. In the present study pigs were inoculated with L. intracellularis and killed from 12 hpi to 5 days post-infection (dpi). The localization of L. intracellularis was determined immunohistochemically and by fluorescence in-situ hybridization. At 12 hpi L. intracellularis was found within epithelial cells at the tips of villi, indicating infection of a range of epithelial cells including mature differentiated enterocytes. Furthermore, early invasion of the intestinal connective tissue was observed; with the presence of single bacteria in the lamina propria 12 hpi, and with a further spread of bacteria in the lamina propria observed at 5 dpi, suggesting an active role for the lamina propria in the course of infection.

摘要

胞内劳森菌是猪增生性肠炎(PE)的病原体,据信它会感染肠道隐窝中具有有丝分裂活性的上皮细胞,然后随着这些细胞分裂在其中繁殖和扩散。感染的进一步传播被认为是通过受感染隐窝中的细菌脱落,随后感染新的隐窝来实现的。PE发病机制的早期阶段,即感染后0至48小时(hpi),尚未在体内进行研究。在本研究中,猪接种了胞内劳森菌,并在感染后12小时至5天(dpi)处死。通过免疫组织化学和荧光原位杂交确定胞内劳森菌的定位。在感染后12小时,在绒毛尖端的上皮细胞内发现了胞内劳森菌,这表明一系列上皮细胞包括成熟分化的肠上皮细胞受到了感染。此外,观察到肠道结缔组织的早期侵袭;在感染后12小时,固有层中有单个细菌存在,在感染后5天观察到细菌在固有层中进一步扩散,这表明固有层在感染过程中发挥了积极作用。

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