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用1型溶血曼氏杆菌野生型或白细胞毒素缺陷突变株经气管内接种SCID - bo和SCID - bg小鼠后的肺部病变

Lung lesions in SCID-bo and SCID-bg mice after intratracheal inoculation with wild-type or leucotoxin-deficient mutant strains of Mannheimia haemolytica serotype 1.

作者信息

Gatto N T, Confer A W, Estes D M, Whitworth L C, Murphy G L

机构信息

Department of Veterinary Pathobiology, 250 McElroy Hall, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK 74078-2007.

出版信息

J Comp Pathol. 2006 May;134(4):355-65. doi: 10.1016/j.jcpa.2006.02.004. Epub 2006 May 19.

Abstract

The purpose of this study was to investigate SCID-bg mice engrafted with bovine haematolymphoid tissues (SCID-bo) as a model for studying bovine Mannheimia haemolytica serotype 1- induced pneumonia, in which leucotoxin (LKT) plays a major role. In experiment A, SCID-bo and SCID-bg mice were inoculated intratracheally with either (1) phosphate-buffered saline (PBS), (2) M. haemolytica wild-type strain 89010807N ("LKT(+)WT"), (3) a M. haemolytica leucotoxin-deficient mutant of strain 89010807N ("LKT(-)mutant"), or (4) the M. haemolytica wild-type Oklahoma strain. Mice were killed for examination at intervals between 20 and 44h after inoculation. Lung lesions consisted of thickened alveolar septa and neutrophil and macrophage infiltrates in the bronchioles and alveoli. Lung lesion scores in the SCID-bo mice inoculated with LKT(+)WT or LKT(-) mutant were significantly (P<0.05) greater than those of the PBS control group, but the two bacterial strains produced results that did not differ significantly. M. haemolytica was isolated from lung, liver and spleen after inoculation but less frequently as time progressed. In experiment B, SCID-bg mice were inoculated intratracheally with live LKT(+)WT or formalin-killed LKT(+)WT and killed 24, 48 or 96 h later. Lung lesions were histologically similar to those observed in experiment A; however, there were no significant differences in the lung lesion scores between groups. It was concluded that the lesions seen in this study were probably not due to LKT, and that the SCID-bo mouse does not provide a good rodent model for bovine pneumonia.

摘要

本研究的目的是调查植入牛血液淋巴组织的重症联合免疫缺陷-bg小鼠(SCID-bo),作为研究由溶血曼氏杆菌1型引起的肺炎的模型,其中白细胞毒素(LKT)起主要作用。在实验A中,给SCID-bo和SCID-bg小鼠经气管内接种以下物质之一:(1)磷酸盐缓冲盐水(PBS),(2)溶血曼氏杆菌野生型菌株89010807N(“LKT(+)WT”),(3)89010807N菌株的溶血曼氏杆菌白细胞毒素缺陷突变体(“LKT(-)突变体”),或(4)溶血曼氏杆菌野生型俄克拉荷马菌株。在接种后20至44小时的间隔时间处死小鼠进行检查。肺部病变包括肺泡间隔增厚以及细支气管和肺泡中的中性粒细胞和巨噬细胞浸润。接种LKT(+)WT或LKT(-)突变体的SCID-bo小鼠的肺部病变评分显著高于(P<0.05)PBS对照组,但这两种菌株产生的结果没有显著差异。接种后从肺、肝和脾中分离出溶血曼氏杆菌,但随着时间的推移分离频率降低。在实验B中,给SCID-bg小鼠经气管内接种活的LKT(+)WT或福尔马林灭活的LKT(+)WT,并在24、48或96小时后处死。肺部病变在组织学上与实验A中观察到的相似;然而,各组之间的肺部病变评分没有显著差异。得出的结论是,本研究中观察到的病变可能不是由LKT引起的,并且SCID-bo小鼠不能提供一个很好的牛肺炎啮齿动物模型。

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