Extensive Mycobacterium bovis BCG infection of liver parenchymal cells in immunocompromised mice.
Extensive Mycobacterium bovis BCG infection of liver parenchymal cells in immunocompromised mice.
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免疫功能低下小鼠的肝实质细胞被牛分枝杆菌 BCG 广泛感染。
DOI：
10.1128/iai.69.5.3175-3180.2001
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发表时间：
2001
影响因子：
3.1
通讯作者：
North,RJ
中科院分区：
文献类型：
--
作者：
Mills,JW;Ryan,L;LaCourse,R;North,RJ
用105CFU牛分枝杆菌BCG静脉感染野生型（WT）、严重联合免疫缺陷（SCID）、醋酸氢化可的松（HC）治疗的WT和HC治疗的SCID小鼠，对其肝脏进行组织学研究。发现SCID小鼠中的感染进展快于WT小鼠，并且HC治疗导致两种类型小鼠中的感染加重。在所有病例中，肝脏感染仅限于主要由巨噬细胞填充的肉芽肿。HC处理的SCID小鼠中较高水平的感染，而不是HC处理的WT小鼠，与肉芽肿边缘的实质细胞的广泛感染和破坏相关。结果表明，在T细胞介导的免疫和HC敏感的T细胞独立的防御机制的情况下，巨噬细胞不能限制BCG的生长和局限于其细胞质的感染。因此，BCG杆菌被释放到细胞外环境中，在那里它们被邻近的实质细胞摄取。
A histologic study was performed on the livers of wild-type (WT), severe combined immunodeficient (SCID), hydrocortisone acetate (HC)-treated WT, and HC-treated SCID mice infected intravenously with 105CFU ofMycobacterium bovisBCG. It was found that infection progressed faster in SCID mice than in WT mice and that HC treatment caused exacerbation of infection in both types of mice. In all cases infection in the liver was confined to granulomas that were populated predominantly by macrophages. Higher levels of infection in HC-treated SCID mice, but not HC-treated WT mice, were associated with extensive infection and destruction of parenchymal cells at the margins of granulomas. The results indicate that in the absence of T-cell-mediated immunity and of HC-sensitive T-cell-independent defense mechanisms, macrophages are incapable of restricting BCG growth and of confining infection to their cytoplasm. Consequently, BCG bacilli are released into the extracellular environment, where they are ingested by neighboring parenchymal cells.