Ritchey J W, Davis M S, Breshears M A, Willard M D, Williamson K K, Royer C M, Payton M E, Cragun A S
Department of Veterinary Pathobiology, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK 74078, USA.
J Comp Pathol. 2011 Jul;145(1):68-76. doi: 10.1016/j.jcpa.2010.11.008. Epub 2011 Jan 17.
Alaskan racing sled dogs are a well-established model of exercise-induced gastric disease. The aim of this study was to define the temporal development of microscopical gastric lesions during long distance racing. Two groups of dogs were examined: group I comprised conditioned dogs that were exercising and group II were conditioned dogs not exercising. The gastric mucosa was examined endoscopically and sampled for routine histopathology and microscopical scoring, immunohistochemistry (IHC) and detection of apoptotic epithelial cells. Overall, group I dogs exhibited more significant epithelial lesions, including ulcers, compared with dogs in group II. Group II dogs exhibited the most severe mucosal inflammatory infiltrates. Although the intensity of inflammation differed, the nature of the inflammation was similar between groups, consisting of diffuse lymphocytic infiltration and a unique interface-type infiltrate that obscured the basement membrane zone and was accompanied by intraepithelial infiltration of lymphocytes. IHC confirmed the presence of CD3(+) T and CD79(+) B lymphocytes within the mucosal infiltrates; however, most of the intraepithelial and interface infiltrates were CD3(+) T cells. Spiral-shaped bacterial organisms were seen in the gastric tissues; however, their presence did not correlate with either the severity of epithelial lesions, inflammation or the pattern of interface inflammation. The number of apoptotic epithelial cells was widely variable and not significantly different between groups. These findings confirm previous observations that gastric ulcers develop in conditioned dogs under racing stress. The unique nature of the interface-type gastric inflammation is similar to that of human lymphocytic gastritis and may suggest an immune-mediated mechanism for the changes seen in Alaskan racing sled dogs.
阿拉斯加雪橇赛犬是运动诱发胃部疾病的成熟模型。本研究的目的是确定长距离比赛期间微观胃部病变的时间发展情况。对两组犬进行了检查：第一组包括正在运动的训练有素的犬，第二组是不运动的训练有素的犬。对胃黏膜进行了内镜检查，并取样进行常规组织病理学检查、微观评分、免疫组织化学（IHC）以及凋亡上皮细胞检测。总体而言，与第二组犬相比，第一组犬表现出更明显的上皮病变，包括溃疡。第二组犬表现出最严重的黏膜炎症浸润。尽管炎症强度不同，但两组之间炎症的性质相似，均由弥漫性淋巴细胞浸润和一种独特的界面型浸润组成，这种浸润模糊了基底膜区，并伴有淋巴细胞的上皮内浸润。免疫组织化学证实黏膜浸润内存在CD3(+) T淋巴细胞和CD79(+) B淋巴细胞；然而，大多数上皮内和界面浸润是CD3(+) T细胞。在胃组织中可见螺旋形细菌生物体；然而，它们的存在与上皮病变的严重程度、炎症或界面炎症模式均无关联。凋亡上皮细胞的数量差异很大，两组之间无显著差异。这些发现证实了先前的观察结果，即在比赛压力下训练有素的犬会出现胃溃疡。界面型胃炎的独特性质与人类淋巴细胞性胃炎相似，这可能提示阿拉斯加雪橇赛犬所出现的变化存在免疫介导机制。
