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细菌清除功能缺陷是导致绵羊感染溶血曼海姆菌肺炎后肺部病变加剧的原因。

Defective bacterial clearance is responsible for the enhanced lung pathology characteristic of Mannheimia haemolytica pneumonia in bighorn sheep.

机构信息

Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, WA 99164-7040, USA.

出版信息

Vet Microbiol. 2011 Dec 15;153(3-4):332-8. doi: 10.1016/j.vetmic.2011.06.008. Epub 2011 Jun 22.

DOI:10.1016/j.vetmic.2011.06.008
PMID:21742446
Abstract

The molecular and cellular basis for the enhanced lung pathology and mortality caused by Mannheimia haemolytica in bighorn sheep (BHS, Ovis canadenesis), in comparison to domestic sheep (DS, Ovis aries), is not clear. Polymorphonuclear leukocytes (PMNs) of BHS are four- to eight-fold more susceptible to M. haemolytica leukotoxin-induced cytolysis, which is likely to reduce the number of functional phagocytes in the lung. We hypothesized that enhanced lung pathology is due to defective clearance of M. haemolytica from the lungs of BHS. To test this hypothesis, M. haemolytica (1 × 10(7) colony forming units [cfu]) were inoculated intra-tracheally into three groups each of BHS and DS, which were euthanized and necropsied at 4, 12, and 18 h post-inoculation (hpi). Bacterial and leukocyte counts were performed on broncho-alveolar lavage fluid (BALF) collected at necropsy. BALF from BHS euthanized at 4 and 12 hpi contained a significantly higher number of M. haemolytica than that from DS. More importantly, DS did not have any bacteria in BALF at 18 hpi, while the BHS still had significant numbers. As expected, the BHS did exhibit more extensive lung lesions at 12 and 18 hpi when compared to DS. At 18 hpi, necrotic PMNs were observed in the lesional lung tissues of BHS, but not DS. Furthermore, BALF from BHS had significantly lower titers of antibodies to Lkt and surface antigens of M. haemolytica, than that of DS. These findings suggest that the enhanced pathology in BHS lungs is due to defective clearance of M. haemolytica from the lungs.

摘要

绵羊肺炎支原体引起的大角羊(BHS,Ovis canadenesis)肺部病变和死亡率增强的分子和细胞基础与绵羊(DS,Ovis aries)相比尚不清楚。BHS 的多形核白细胞(PMN)对绵羊肺炎支原体白细胞毒素诱导的细胞溶解的敏感性高 4-8 倍,这可能会减少肺部功能吞噬细胞的数量。我们假设增强的肺部病理学是由于 BHS 肺部清除绵羊肺炎支原体的功能缺陷所致。为了验证这一假设,我们将绵羊肺炎支原体(1×10(7)个菌落形成单位 [cfu])气管内接种到每组 3 只 BHS 和 DS 中,然后在接种后 4、12 和 18 小时安乐死并进行尸检。在尸检时收集支气管肺泡灌洗液(BALF)并进行细菌和白细胞计数。BHS 安乐死 4 和 12 小时的 BALF 中含有明显更高数量的绵羊肺炎支原体,而 DS 的 BALF 中则没有。更重要的是,DS 在 18 小时时 BALF 中没有任何细菌,而 BHS 中仍然有大量细菌。如预期的那样,与 DS 相比,BHS 在 12 和 18 小时时肺部病变更广泛。在 18 小时时,BHS 的病变肺组织中观察到坏死的 PMN,但在 DS 中则没有。此外,BHS 的 BALF 对 Lkt 和绵羊肺炎支原体表面抗原的抗体滴度明显低于 DS。这些发现表明,BHS 肺部的增强病理学是由于从肺部清除绵羊肺炎支原体的功能缺陷所致。

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