Rojas-Espinosa O, Vega R, Oltra A, Arce P, Nunez A
Department of Immunology, National School of Biological Sciences, National Polytechnic Institute, México, D.F.
Int J Lepr Other Mycobact Dis. 1988 Sep;56(3):428-36.
A kinetic study on the evolution of granulomas that appear in the liver of NIH mice inoculated with 10(8) Mycobacterium lepraemurium by the intraperitoneal route has been performed. The liver was chosen because of its nonlymphoid histology which allowed us to visualize the appearance and maturation of the cell infiltrates generated as a consequence of the mycobacterial infection. The study analyzed both the macrophage activation within the granulomas and the fate of bacilli within the macrophage. The results showed that this mycobacteriosis induces a relatively early macrophage activation (a very likely result of a cell-mediated immune response triggered by the bacilli) that peaks between 45 and 60 days postinoculation, fades thereafter, and practically disappears several days later. Bacilli are susceptible to the microbicidal effects of activated macrophages, but when the macrophages are turned off (probably due to active suppressive mechanisms), the surviving bacilli reinitiate the infection with no further macrophage opposition. As a result, more phagocytes are attracted to the infection sites and the cell infiltrates grow steadily to become confluent, increasing the granuloma fraction and eventually replacing the liver parenchyma. The findings suggest that in murine "leprosy" infection, early immunological changes occur that enable the macrophages present in the granulomas to kill the infecting M. lepraemurium regardless of the eventual lepromatoid evolution of the granulomas. Lepromatoid granulomas in the mouse and lepromatous granulomas in man are equivalent structures in regard to their histology and bacteriology.
对通过腹腔途径接种10(8) 条鼠麻风杆菌的NIH小鼠肝脏中出现的肉芽肿演变进行了动力学研究。选择肝脏是因为其非淋巴组织学特性，这使我们能够观察到由分枝杆菌感染产生的细胞浸润的出现和成熟过程。该研究分析了肉芽肿内巨噬细胞的激活情况以及巨噬细胞内杆菌的命运。结果表明，这种分枝杆菌病诱导相对早期的巨噬细胞激活（很可能是由杆菌触发的细胞介导免疫反应的结果），在接种后45至60天达到峰值，此后逐渐消退，并在几天后几乎消失。杆菌易受活化巨噬细胞的杀菌作用影响，但当巨噬细胞失活（可能是由于活跃的抑制机制）时，存活的杆菌会重新引发感染，且不再受到巨噬细胞的抵抗。结果，更多的吞噬细胞被吸引到感染部位，细胞浸润稳定增长并融合，增加了肉芽肿比例，最终取代肝实质。研究结果表明，在鼠类“麻风”感染中，会发生早期免疫变化，使肉芽肿中的巨噬细胞能够杀死感染的鼠麻风杆菌，而不论肉芽肿最终的瘤型演变如何。就组织学和细菌学而言，小鼠的瘤型肉芽肿和人类的瘤型肉芽肿是等效结构。
