McBride J W, Wozniak E J, Brewer A W, Naydan D K, Osburn B I
School of Veterinary Medicine, University of California, Davis, CA 95616, USA.
Microb Pathog. 1999 Apr;26(4):183-93. doi: 10.1006/mpat.1998.0266.
The pathogenesis of bovine pneumonic pasteurellosis is not completely understood, and studies have not established that Pasteurella haemolytica A1 (Ph1) virulence is exclusively responsible for the development of acute pulmonary lesions. The purpose of this investigation was to determine if immune complex disease is involved in the pathogenesis of bovine pneumonic pasteurellosis. A retrospective immunohistologic study of lung tissue from natural cases of bovine pneumonic pasteurellosis (44) as performed, and immune complexes were observed in alveloar spaces and walls in 88% of these cases. To study this pathologic mechanism experimentally, groups of mice were immunized with purified Ph1 outer membranes (OMs) or sham immunized on days 0 and 14. Mice were challenged intratracheally on day 24 with either live Ph1 or Ph1 OMs, and pulmonary lesions were assessed 24 h after challenge. Placebo immunized mice developed focal infiltrates of neutrophils and macrophages centered around large caliber bronchi. Mice immunized with Ph1 OMs and challenged with live Ph1 or OMs developed severe bronchointerstitial pneumonia with diffuse neutrophilic infiltration, focal necrosis, hemorrhage and edema, that is histologically similar to bovine pneumonic pasteurellosis. Immunohistology revealed flocculent aggregates of IgG and complement positive material within alveolar spaces and walls from mice challenged with live Ph1, and fine granular deposits of IgG and complement positive material were observed lining the alveolar walls from mice challenged with Ph1 OMs. Immunized mice exhibited high serum IgG antibody titers to Ph1 outer membrane proteins (OMPs). Results of this study suggest that immune complex disease plays a role in the pathogenesis of bovine pneumonic pasteurellosis.
牛肺炎性巴氏杆菌病的发病机制尚未完全明确,而且研究尚未证实溶血巴氏杆菌A1型(Ph1)的毒力是急性肺部病变发生的唯一原因。本研究的目的是确定免疫复合物疾病是否参与牛肺炎性巴氏杆菌病的发病机制。对44例自然发生的牛肺炎性巴氏杆菌病病例的肺组织进行了回顾性免疫组织学研究,在88%的病例中,肺泡腔和肺泡壁中观察到了免疫复合物。为了通过实验研究这一病理机制,在第0天和第14天,给几组小鼠分别免疫纯化的Ph1外膜(OMs)或进行假免疫。在第24天,给小鼠气管内接种活的Ph1或Ph1 OMs,接种后24小时评估肺部病变。接种安慰剂的小鼠出现了以大口径支气管为中心的中性粒细胞和巨噬细胞局灶性浸润。用Ph1 OMs免疫并接种活的Ph1或OMs的小鼠发生了严重的支气管间质性肺炎,伴有弥漫性中性粒细胞浸润、局灶性坏死、出血和水肿,在组织学上与牛肺炎性巴氏杆菌病相似。免疫组织学显示,接种活Ph1的小鼠肺泡腔和肺泡壁内有IgG和补体阳性物质的絮状聚集物,接种Ph1 OMs的小鼠肺泡壁内衬有IgG和补体阳性物质的细颗粒沉积物。免疫小鼠对Ph1外膜蛋白(OMPs)表现出高血清IgG抗体滴度。本研究结果表明,免疫复合物疾病在牛肺炎性巴氏杆菌病的发病机制中起作用。