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小鼠经胃内感染后瘙痒病的发病机制。

Pathogenesis of scrapie in mice after intragastric infection.

作者信息

Kimberlin R H, Walker C A

机构信息

Institute for Animal Health, AFRC & MRC Neuropathogenesis Unit, Edinburgh, U.K.

出版信息

Virus Res. 1989 Mar;12(3):213-20. doi: 10.1016/0168-1702(89)90040-3.

Abstract

Infection via the gastrointestinal tract is likely to be a natural route of scrapie infection in sheep. This paper describes the pathogenesis of the 139A strain of scrapie introduced intragastrically (i.g.) into CW mice. There was an almost immediate uptake of infectivity and onset of replication in Peyer's patches which preceded replication in spleen. Splenectomy had no effect on incubation period suggesting that, in contrast to the intraperitoneal route, the spleen plays little or no role in the pathogenesis of 139A scrapie administered intragastrically. Replication in the CNS was first detectable in the thoracic spinal cord and later in brain. The evidence is consistent with neural spread of infection from the gastrointestinal tract, via the enteric and sympathetic nervous systems to spinal cord. Neuroinvasion may be initiated either via infection of Peyer's patches or directly by infection of nerve endings in the gut wall. The latter possibility means that pathogenesis may be completely independent of the lymphoreticular system.

摘要

经胃肠道感染很可能是绵羊感染痒病的自然途径。本文描述了经胃内(i.g.)接种到CW小鼠体内的139A株痒病的发病机制。感染性物质几乎立即被摄取,并在派尔集合淋巴结中开始复制,这先于在脾脏中的复制。脾切除术对潜伏期没有影响,这表明与腹腔内途径不同,脾脏在经胃内接种139A痒病的发病机制中作用很小或没有作用。中枢神经系统中的复制首先在胸段脊髓中检测到,随后在脑中检测到。证据表明感染是从胃肠道经肠神经系统和交感神经系统向脊髓进行神经传播。神经侵袭可能通过派尔集合淋巴结感染或直接通过肠壁神经末梢感染引发。后一种可能性意味着发病机制可能完全独立于淋巴网状系统。

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