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关于乳鼠中不存在肠道适应性机制以补偿微小隐孢子虫诱导的氨基酸吸收不良的证据。

Evidence for the absence of an intestinal adaptive mechanism to compensate for C. parvum-induced amino acid malabsorption in suckling rats.

作者信息

Topouchian A, Huneau J F, Barbot L, Rome S, Gobert J G, Tomé D, Kapel N

机构信息

Laboratoire de Biologie Animale et Parasitaire, Faculté des Sciences Pharmaceutiques et Biologiques, Université René Descartes, 75006 Paris, France.

出版信息

Parasitol Res. 2003 Oct;91(3):197-203. doi: 10.1007/s00436-003-0956-9. Epub 2003 Aug 16.

Abstract

In order to assess the impact of Cryptosporidium parvum on host intestinal physiology, we investigated absorption of the two principal amino acids in dam's milk (leucine, glutamate), using Ussing chambers and RT-PCR analyses. Experiments were performed in both heavily (ileum) and mildly (duodenum) infected segments of the small intestine at the peak of infection [day 8 post-infection (PI)] and after spontaneous clearance of the parasite (day 17 PI). At day 8 PI, amino acid fluxes across the mucosa were decreased throughout the small intestine (P<0.01) and EAAT3 mRNA expression was reduced ( from -49% to -28%). At day 17 PI, leucine and glutamate fluxes were normalized but the decrease in EAAT3 mRNA levels persisted (from -31% to -46%). Our results demonstrate that cryptosporidiosis induces major amino acid malabsorption involving the entire small intestine which is not counterbalanced by any up-regulation, even after spontaneous clearance of the parasite.

摘要

为了评估微小隐孢子虫对宿主肠道生理的影响,我们使用尤斯灌流小室和逆转录聚合酶链反应分析,研究了母乳中两种主要氨基酸(亮氨酸、谷氨酸)的吸收情况。在感染高峰期(感染后第8天)以及寄生虫自然清除后(感染后第17天),在小肠严重感染段(回肠)和轻度感染段(十二指肠)进行了实验。在感染后第8天,整个小肠黏膜的氨基酸通量均降低(P<0.01),且EAAT3信使核糖核酸表达减少(从-49%降至-28%)。在感染后第17天,亮氨酸和谷氨酸通量恢复正常,但EAAT3信使核糖核酸水平的降低仍然存在(从-31%降至-46%)。我们的结果表明,隐孢子虫病会导致涉及整个小肠的主要氨基酸吸收不良,即使在寄生虫自然清除后,也没有任何上调来抵消这种情况。

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