Butzner J D, Gall D G
Intestinal Diseases Research Unit, University of Calgary, Alberta, Canada.
Pediatr Res. 1988 Apr;23(4):408-13. doi: 10.1203/00006450-198804000-00014.
The aim of this study was to determine if recovery of intestinal function in infant rabbits subjected to protein-calorie malnutrition was delayed as a result of inflammatory injury induced by an experimental bacterial enteritis. Rabbits were malnourished by expanding litter size at 7 days of age and infecting undernourished animals and dietary controls with Yersinia enterocolitica at either 17 or 21 days of age. Intestinal morphology and function were evaluated in infected and noninfected animals from both dietary groups at 27 days of age. Undernutrition alone significantly reduced animal weight, small intestinal weight, segmental jejunal and ileal mucosal weight, villus height, crypt depth, disaccharidase activities, mucosal protein and DNA contents, but increased ileal short-circuited glucose-stimulated Na+ absorption compared to controls. The jejunum of undernourished rabbits at 6 days postinfection exhibited an intestinal injury, as evidenced by a mild inflammatory infiltrate and further reductions in villus height, mucosal weight, lactase activity, protein and DNA content, not seen in infected dietary controls. Jejunal recovery was complete by 10 days postinfection. In the ileum of infected animals of both dietary groups at 6 days post-infection, a severe inflammatory response, decreased villus height, elongated crypts, and depressed stimulation of Na+ absorption by glucose was observed. By 10 days after infection, while recovery was nearly complete in dietary controls, intestinal damage persisted in the undernourished rabbits, as evidenced by absent glucose-stimulated Na+ absorption, continued severe inflammation and microabscess formation. We conclude that intestinal injury is more severe and chronic in the undernourished, compared to dietary control infant rabbits subjected to an acute bacterial enteritis.
本研究的目的是确定蛋白质 - 热量营养不良的幼兔肠道功能的恢复是否因实验性细菌性肠炎诱导的炎症损伤而延迟。通过在7日龄时扩大窝仔数使兔子营养不良,并在17日龄或21日龄时用小肠结肠炎耶尔森菌感染营养不良的动物和饮食对照组。在27日龄时评估两个饮食组中感染和未感染动物的肠道形态和功能。与对照组相比,仅营养不良就显著降低了动物体重、小肠重量、空肠和回肠节段黏膜重量、绒毛高度、隐窝深度、双糖酶活性、黏膜蛋白和DNA含量,但增加了回肠短路葡萄糖刺激的Na +吸收。感染后6天,营养不良兔子的空肠出现肠道损伤,表现为轻度炎症浸润以及绒毛高度、黏膜重量、乳糖酶活性、蛋白和DNA含量进一步降低,而感染的饮食对照组未见此现象。感染后10天空肠恢复完成。在感染后6天,两个饮食组感染动物的回肠均观察到严重的炎症反应、绒毛高度降低、隐窝延长以及葡萄糖对Na +吸收的刺激减弱。感染后10天,虽然饮食对照组的恢复几乎完成,但营养不良兔子的肠道损伤仍然存在,表现为葡萄糖刺激的Na +吸收缺失、持续的严重炎症和微脓肿形成。我们得出结论,与遭受急性细菌性肠炎的饮食对照幼兔相比,营养不良幼兔的肠道损伤更严重且更持久。