Turner J, Frank A A, Brooks J V, Marietta P M, Orme I M
Departments of Microbiology and Pathology, Colorado State University, Fort Collins, CO, USA.
Immunology. 2001 Feb;102(2):248-53. doi: 10.1046/j.1365-2567.2001.01161.x.
It is well established in animal models that production of the cytokine tumour necrosis factor-alpha (TNF-alpha) is essential to the proper expression of acquired specific resistance following infection with Mycobacterium tuberculosis. This gives rise to an apparent state of chronic disease which over the next 100-200 days is characterized by slowly worsening pathological changes in the lung. To determine whether continued TNF-alpha production was harmful during this phase mice were treated with a TNF-alpha inhibitor, pentoxifylline. It was observed that although this therapy did not alter the numbers of bacteria recovered from the lungs of the infected mice, tissue damage within the lung was accelerated. These data thus demonstrate that production of TNF-alpha, already known to be important during the early expression of resistance to tuberculosis, remains important and beneficial during the chronic stage of the disease.
在动物模型中已充分证实，细胞因子肿瘤坏死因子-α（TNF-α）的产生对于结核分枝杆菌感染后获得性特异性抵抗力的正常表达至关重要。这会引发一种明显的慢性病状态，在接下来的100 - 200天里，其特征是肺部病理变化逐渐恶化。为了确定在此阶段持续产生TNF-α是否有害，用TNF-α抑制剂己酮可可碱对小鼠进行治疗。观察到，尽管这种治疗并未改变从感染小鼠肺部回收的细菌数量，但肺部的组织损伤却加速了。因此，这些数据表明，TNF-α的产生在已知对结核病抵抗力早期表达很重要的同时，在疾病的慢性阶段仍然重要且有益。
