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首页> 外文期刊>Life sciences >Viral neuroinvasion as a marker for BBB integrity following exposure to cholinesterase inhibitors.
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Viral neuroinvasion as a marker for BBB integrity following exposure to cholinesterase inhibitors.

机译：暴露于胆碱酯酶抑制剂后，病毒神经入侵可作为BBB完整性的标志物。

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Exposure to the nerve agent soman, an irreversible cholinesterase (ChE) inhibitor, results in changes in blood-brain barrier permeability attributed to its seizure-induced activity. However, smaller BBB changes may be independent of convulsions. Such minor injury may escape detection. A nonneuroinvasive neurovirulent Sindbis virus strain (SVN) was used as a marker for BBB permeability. Peripheral inoculation of mice with 2 x 10(3) plaque forming units (PFU) caused up to 10(5) PFU/ml viremia after 24 hours with no signs of central nervous system (CNS) infection and with no virus detected in brain tissue. Intra-cerebral injection of as low as 1-5 PFU of the same virus caused CNS infection, exhibited 5-7 days later as hind limb paralysis and death. Soman (0.1-0.7 of the LD50) was administered at peak viremia (1 day following peripheral inoculation). Sublethal soman exposure at as low as 0.1 LD50 resulted in CNS infection 6-8 days following inoculation in 30-40% of the mice. High virus titer were recorded in brain tissue of sick mice while no virus was detected in healthy mice subjected to the same treatment. No changes in the level of viremia or changes in viral traits were observed in the infected mice. The reversible anticholinesterases physostigmine (0.2 mg/kg, s.c.) and pyridostigmine (0.4 mg/kg, i.m.) injected at a dose equal to 0.1 LD50, induced similar results. Thus, both central and peripheral anticholinesterases (anti-ChEs) induce changes in BBB permeability sufficient to allow, at least in some of the mice, the invasion of this otherwise noninvasive but highly neurovirulent virus. This BBB change is probably due to the presence of cholinesterases in the capillary wall. SVN brain invasion served here as a highly sensitive and reliable marker for BBB integrity.
机译：暴露于神经药物梭曼（一种不可逆的胆碱酯酶（ChE）抑制剂）会导致血脑屏障通透性发生变化，这归因于其癫痫发作诱导的活性。但是，较小的血脑屏障变化可能与抽搐无关。这样的轻伤可能无法发现。非神经侵入性神经毒性辛德比斯病毒株（SVN）被用作BBB通透性的标志物。小鼠周围接种2 x 10（3）噬菌斑形成单位（PFU），在24小时后引起高达10（5）PFU / ml病毒血症，无中枢神经系统（CNS）感染迹象，并且在脑组织中未检测到病毒。脑内注射低至1-5 PFU的同一病毒会引起CNS感染，在5-7天后表现为后肢麻痹和死亡。 Soman（LD50的0.1-0.7）在病毒血症高峰期（外周接种后1天）给药。亚致死性梭曼暴露低至0.1 LD50，接种30-40％的小鼠后6-8天导致CNS感染。在患病小鼠的脑组织中记录到较高的病毒滴度，而在接受相同处理的健康小鼠中未检测到病毒。在感染的小鼠中未观察到病毒血症水平或病毒性状的变化。以等于0.1 LD50的剂量注射的可逆抗胆碱酯酶毒扁豆碱（0.2 mg / kg，皮下注射）和吡啶斯的明（0.4 mg / kg，i.m。）引起相似的结果。因此，中枢和外周抗胆碱酯酶（抗ChEs）都诱导BBB通透性的变化，足以至少在某些小鼠中侵入这种原本非侵入性但高度神经毒性的病毒。这种BBB变化可能是由于毛细管壁中存在胆碱酯酶。 SVN脑部入侵是BBB完整性的高度敏感和可靠的标记。

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