Cheville N F, Hostetter J, Thomsen B V, Simutis F, Vanloubbeeck Y, Steadham E
Department of Veterinary Pathology, Iowa State University, Ames, Iowa, USA.
Dtsch Tierarztl Wochenschr. 2001 Jun;108(6):236-43.
The granulomatous enteric lesions of cattle with Johne's disease are composed of infected macrophages, and grow by accumulation, re-infection, and expansion of macrophage populations in the intestinal wall. We have examined the growth of bacteria in macrophages to define characteristics of intracellular trafficking for exocytosis, replication, and antigen presentation. Using immunocytochemical markers for light, confocal and electron microscopy, we have examined potential pathway tropisms using data for bacterial attachment, phagosomal acidification, phagolysosomal degradation and apoptosis. Our hypotheses are that pathogenic/wild-type strains block phagosomal acidification so that the phagosome fails to obtain markers of the late phagosome and phagolysosome, and this leads to the replication pathway within bacteriophorous vacuoles. Non-pathogenic strains appear to be processed to exocytosis, and avirulent mutant strains may be degraded and have preference of antigen processing pathways that involve transport vesicles bearing MHC II antigens. Pathogenicity in a nude mouse model of intestinal infection reveals lesion development and confirms pathway preferences of virulent strains for bacteriophorous vacuole formation.
患有副结核的牛的肉芽肿性肠道病变由受感染的巨噬细胞组成，并通过肠壁中巨噬细胞群体的积累、再感染和扩张而生长。我们研究了巨噬细胞中细菌的生长情况，以确定胞吐、复制和抗原呈递的细胞内运输特征。使用免疫细胞化学标记物进行光学、共聚焦和电子显微镜检查，我们利用细菌附着、吞噬体酸化、吞噬溶酶体降解和细胞凋亡的数据研究了潜在的途径嗜性。我们的假设是，致病/野生型菌株会阻止吞噬体酸化，从而使吞噬体无法获得晚期吞噬体和吞噬溶酶体的标记物，这导致了含菌液泡内的复制途径。非致病菌株似乎会被加工用于胞吐，无毒突变菌株可能会被降解，并优先选择涉及携带MHC II抗原的运输囊泡的抗原加工途径。肠道感染裸鼠模型中的致病性揭示了病变发展，并证实了有毒力菌株对含菌液泡形成的途径偏好。
