Labrec E H, Schneider H, Magnani T J, Formal S B
Department of Applied Immunology, Walter Reed Army Institute of Research, Washington, D.C.
J Bacteriol. 1964 Nov;88(5):1503-18. doi: 10.1128/jb.88.5.1503-1518.1964.
LaBrec, Eugene H., Herman Schneider, Thomas J. Magnani, and Samuel B. Formal. Epithelial cell penetration as an essential step in the pathogenesis of bacillary dysentery. J. Bacteriol. 88:1503-1518. 1964.-A parent strain of Shigella flexneri 2a and a colonial mutant derived from it were studied in three animal models. Both strains were equally virulent for mice when living cells suspended in hog gastric mucin were injected by the intraperitoneal route. Feeding the parent strain to starved guinea pigs, followed by the intraperitoneal injection of opium, resulted in the formation of ulcerative lesions in the intestinal tract and in the death of these animals. When the colonial variant was fed to similarly prepared animals, the animals survived and the intestinal tract remained normal. The parent produced diarrheal symptoms and intestinal lesions after its oral administration to rhesus monkeys; the variant caused neither symptoms nor pathology in this species. Studies were carried out to define the characteristics present in the parent strain and absent in the colonial mutant, which would enable the parent to produce ulcerative lesions of the bowel and death in the guinea pig model or intestinal lesions and diarrheal symptoms in the monkey. Neither serological studies nor growth studies conducted both in vitro and in vivo offered a clue to explain this difference. The virulent parent strain was shown to penetrate the bowel epithelium and enter the lamina propria; the avirulent mutant did not do this. Entrance to the lamina propria was by way of the epithelial cell of the mucosa. The avirulent mutant did not possess the capacity to penetrate this cell. This observation was extended to show that the virulent parent possesses the ability to infect and multiply within HeLa cells; furthermore, the organisms are able to penetrate epithelial cells of the guinea pig cornea, causing ulcerative lesions. The avirulent variant possesses neither of these capacities. It is suggested that epithelial cell penetration is a major factor in determining the pathogenicity of dysentery bacilli.
拉布雷克，尤金·H.，赫尔曼·施耐德，托马斯·J. 马尼亚尼，以及塞缪尔·B. 福尔马尔。上皮细胞穿透作为杆菌性痢疾发病机制中的一个关键步骤。《细菌学杂志》88:1503 - 1518。1964年。——对弗氏志贺菌2a的一个亲代菌株及其衍生的一个菌落突变体在三种动物模型中进行了研究。当将悬浮于猪胃粘蛋白中的活细胞通过腹腔途径注射时，这两种菌株对小鼠的毒力相同。将亲代菌株喂给饥饿的豚鼠，随后腹腔注射鸦片，导致肠道形成溃疡性病变并使这些动物死亡。当将菌落变体喂给同样处理的动物时，动物存活且肠道保持正常。亲代菌株经口给予恒河猴后会产生腹泻症状和肠道病变；变体在该物种中既不引起症状也不导致病理变化。开展研究以确定亲代菌株中存在而菌落突变体中不存在的特征，这些特征使得亲代菌株能够在豚鼠模型中产生肠道溃疡性病变和死亡，或在猴子中产生肠道病变和腹泻症状。无论是血清学研究还是在体外和体内进行的生长研究都未能提供解释这种差异的线索。已表明有毒力的亲代菌株能穿透肠上皮并进入固有层；无毒力的突变体则不能。进入固有层是通过黏膜的上皮细胞。无毒力的突变体不具备穿透这种细胞的能力。这一观察结果进一步表明，有毒力的亲代菌株具有在海拉细胞内感染和繁殖的能力；此外，这些细菌能够穿透豚鼠角膜的上皮细胞，导致溃疡性病变。无毒力的变体不具备这两种能力。有人提出上皮细胞穿透是决定痢疾杆菌致病性的一个主要因素。
