Uhnoo I S, Freihorst J, Riepenhoff-Talty M, Fisher J E, Ogra P L
Department of Pediatrics, State University of New York, Buffalo.
Pediatr Res. 1990 Feb;27(2):153-60. doi: 10.1203/00006450-199002000-00014.
Intestinal absorption of ovalbumin (OVA), a dietary macromolecule, was studied in malnourished and normally nourished suckling mice after experimentally induced infection with rotavirus. All mice developed diarrhea within 24 to 48 h postinoculation. The malnourished animals exhibited more severe symptoms and an increased number of rotavirus-containing enterocytes in intestinal sections as compared to well-nourished mice when examined 3 d postinoculation, at the peak of diarrhea. Histopathologic examination revealed villus atrophy and pronounced vacuolization of villus enterocytes in association with malnutrition and rotavirus infection. The combination of malnutrition and viral infection resulted in more severe mucosal damage, including disruption of microvillus borders. After a single oral dose of 100 micrograms OVA at 3 d postinoculation, the concentration of OVA in serum, gastric content, intestinal lavage fluid, and intestinal tissue homogenates was measured at different time intervals. The concentrations of OVA in intestinal tissue were significantly higher in malnourished animals, whereas lower values were found in rotavirus-infected animals. In all mice, OVA was rapidly absorbed and could be consistently detected in the serum within 5 min. OVA levels peaked at 45 to 60 min and then gradually declined. In malnourished infected animals, the uptake of OVA was rapid and resulted in significantly higher serum levels when compared to well nourished or uninfected controls, respectively. The peak uptake of OVA per g body wt was about 4.5 times more in malnourished infected compared to well-nourished infected mice and 2.5 times higher in normally nourished infected animals when compared to uninfected controls. These results indicate that rotavirus infection in association with malnutrition may cause a significant rise in gut permeability to environmental macromolecules.
在给营养不良和营养正常的乳鼠实验性接种轮状病毒后，研究了膳食大分子卵清蛋白（OVA）的肠道吸收情况。所有小鼠在接种后24至48小时内均出现腹泻。在接种后3天腹泻高峰期检查时，与营养良好的小鼠相比，营养不良的动物表现出更严重的症状，并且肠道切片中含轮状病毒的肠细胞数量增加。组织病理学检查显示，与营养不良和轮状病毒感染相关的绒毛萎缩和绒毛肠细胞明显空泡化。营养不良和病毒感染共同导致更严重的黏膜损伤，包括微绒毛边界的破坏。在接种后3天单次口服100微克OVA后，在不同时间间隔测量血清、胃内容物、肠灌洗液和肠组织匀浆中OVA的浓度。营养不良动物的肠组织中OVA浓度显著更高，而在轮状病毒感染的动物中则发现较低的值。在所有小鼠中，OVA迅速被吸收，并且在5分钟内可在血清中持续检测到。OVA水平在45至60分钟达到峰值，然后逐渐下降。在营养不良的感染动物中，OVA的摄取迅速，与营养良好或未感染的对照组相比，血清水平显著更高。与营养良好的感染小鼠相比，营养不良的感染小鼠每克体重OVA的峰值摄取量大约高4.5倍，与未感染的对照组相比，正常营养的感染动物高2.5倍。这些结果表明，轮状病毒感染与营养不良可能导致肠道对环境大分子的通透性显著增加。
